Volume 202, Issue 2 , Pages 103-123, February 2010
Paternal factors and low birthweight, preterm, and small for gestational age births: a systematic review
Article Outline
- Abstract
- Materials and Methods
- Results
- Comment
- Acknowledgments
- Appendix
- References
- Copyright
A systematic review of the risks of a low birthweight (LBW), preterm, and small-for-gestational-age births in relation to paternal factors was performed. Medline, Embase, Cumulative Index of Nursing and Allied Health Literature, and bibliographies of identified articles were searched for English-language studies. Study qualities were assessed according to a predefined checklist. Thirty-six studies of low-to-moderate risk of bias were reviewed for various paternal factors: age, height, weight, birthweight, occupation, education, and alcohol use. Extreme paternal age was associated with higher risk for LBW. Among infants who were born to tall fathers, birthweight was approximately 125-150 g higher compared with infants who were born to short fathers. Paternal LBW was associated with lower birthweight of the offspring. In conclusion, paternal characteristics including age, height, and birthweight are associated with LBW. Paternal occupational exposure and low levels of education may be associated with LBW; however, further studies are needed.
Key words: anthropometry, intergenerational effects, paternal age, paternal birthweight, paternal occupation
Low birthweight (LBW) birth and preterm births (PTBs) are public health issues with significant individual, familial, and societal impact. Familial influence in the cause of LBW/PTB births is suspected; however, the major research attention has been focused on maternal determinants. Paternal factors (such as advanced paternal age1 and chemical exposures) have been linked with congenital malformations. De La Rochebrochard et al,2 in a minireview, concluded that advanced paternal age (>40 years) was associated with miscarriages and fetal deaths. Diseases such as Alpert syndrome, Marfan syndrome, and Waardenberg syndrome are associated with advanced paternal age. Strobino et al3 reviewed the connection between paternal occupational exposure and effect on offspring. They reported that paternal occupation was not associated with spontaneous abortion and that there was a lack of conclusive impact on other birth outcomes.
For Editors' Commentary, see Table of Contents
See related editorial,page 99
Studies have reported paternal factors that influence birthweight or gestational age. However, no comprehensive review of paternal determinants or factors on LBW, PTB, or small for gestational age (SGA) births has been conducted. The objective of this study was to review systematically the risk of an infant with LBW, PTB, and SGA in relation to various reported paternal factors.
Materials and Methods
The data were extracted from published articles; therefore, no ethical approval was obtained.
Criteria for consideration of studies for this review
Observational studies that explored the association of any of the paternal factors and the outcomes of LBW, PTB, and SGA births of offspring were included in this review. If the study provided adequate information on the method of ascertainment of the paternal factor and its effects on any of the outcomes of interest, the study was eligible for inclusion in the review. We included only information that was available from the publications and did not contact primary authors. Studies that were published as abstracts were excluded.
Types of studies
Observational cohort studies, case control studies, and studies of surveys or interviews were included. Reports of data from national or local vital statistics that were not published as peer-reviewed articles were not included.
Types of participants
Women who had a live birth were included. Data on reports of maternal influence on birth outcomes were not included in this review.
Assessment of exposure
Previous knowledge of the subject indicated that paternal age, anthropometry, paternal birthweight, occupation, and educational background would be probable exposures to be included in the review.4 We did not include paternal race as an exposure variable because race has a complex interaction with maternal race. Similarly, we excluded paternal smoking as an exposure because most studies have reported on environmental tobacco exposure, which could have been from partners or other sources, and it was difficult to differentiate. We included studies that reported a collection of ascertainment of exposure data from maternal charts, interview, and direct or indirect assessments.
Types of outcome measures
Studies that reported data on any of the following outcomes were included: (1) LBW birth defined as birthweight <2.5 kg; (2) PTB defined as gestational age <37 weeks; (3) birthweight in grams; (4) gestational age in weeks, and (5) SGA birth defined as birthweight <10th percentile for gestational age.
Search strategy for identification of studies
Electronic databases (Medline, Embase, and Cumulative Index of Nursing and Allied Health Literature) were searched, with assistance from an experienced librarian, from their inception to March 2009 for all published studies in the English language. The search terms were modified according to database requirements. The reference lists of the identified articles were reviewed to locate additional eligible studies. The articles were scanned initially on the basis of titles and abstracts. The reviewer was not blinded to authors or institution. Selected articles were retrieved in full and were assessed for eligibility. Search terms used were low birthweight; premature birth; preterm birth; small for gestational age; growth, intrauterine; growth restriction, fetal; growth restriction, intrauterine; high risk pregnancy; infant, premature; infant, newborn; pregnancy; familial factors; father, paternal factors, paternal age, paternal birthweight, occupation, education, anthropometry, weight, height, body mass, and body mass index.
Methods of the review
Data extraction
Data from each eligible study were extracted into custom-made data collection forms. Minor modifications (such as combining birthweight means for male and female subjects) and the calculation of raw percentages from available data were done. Confounders that were adjusted for in the analyses in the individual studies were reported. When adjusted data were reported in the primary studies, they were extracted and noted in the results.
Assessment of quality of included studies
The methodologic quality of studies was assessed with a predefined checklist that was based on criteria for the sample selection, exposure assessment, outcome assessment, confounder, and analytical and attrition biases (Appendix). The classifications were applied in each category: cannot tell, no bias, low risk, moderate risk, or high risk of bias.
Data synthesis
We expected a significant degree of clinical heterogeneity among studies in each of the paternal factors and planned for a systematic review and not metaanalyses from the outset. Qualitative synthesis of the evidence was planned because of the reasons mentioned earlier.
Heterogeneity and publication bias assessment
Clinical heterogeneity was assessed and reported in the Tables.
Results
Description of studies
Thirty-eight studies were included in this review.5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42 Some of the included studies reported on >1 paternal factor. Paternal alcohol use was identified as an exposure during the literature review (which was not planned a priori). Eleven studies were excluded after detailed evaluation. Details of included studies and reasons for excluded studies are given in Figure 1.43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53

FIGURE 1.
Flow diagram of included studies.
SGA, small for gestational age.
Shah. Paternal factors and LBW/PTB. Am J Obstet Gynecol 2010.
Methodologic quality of included studies
The results of the quality assessments of the included studies are reported in TABLE 1, TABLE 2, TABLE 3, TABLE 4, TABLE 5, TABLE 6. The studies had low-to-moderate risk of biases. The major criticism of the included studies was that the assessment of exposure in many reports was indirect (such as maternal history, derived or deduced assessment method for occupational exposure). Adjustment of confounders was variable among studies; however, compared with other reports of determinants of LBW/PTB births, most of the studies in this category have accounted for common confounders. Assessment of outcomes was satisfactory in most studies. Many studies reported only incidence or percentage of outcome data and not odds ratio or relative risk and their associated confidence interval. The data in the Tables reflect what is reported in the articles. If the risk estimates are missing from a Table, the implication is that they were not reported.
TABLE 1. Paternal age and relation to low birthweight, preterm, and small-for-gestational-age births
| Study | Study characteristics | Assessment | Risk of bias | Results | |||
|---|---|---|---|---|---|---|---|
| Category, y | LBW, OR (95% CI) | PTB, OR (95% CI) | SGA, OR (95% CI) | ||||
| Abel et al5,a | 1978-1992; Cohort study performed in North Dakota; used the statewide database; n = 154,391 | Exposure: maternal history | Selection: none | 21-26 | 1.00 | 1.00 | |
| Outcome: birth certificates | Exposure assessment: low | <20 | 1.28 | 1.24 | |||
| Confounders adjusted: socioeconomic status, maternal age, infant sex, race | Outcome assessment: none | 26-30 | 1.07 | 0.89 | |||
| Confounding factors: low | 31-35 | 1.03 | 0.88 | ||||
| Analytical: none | 36-40 | 1.26 | 1.01 | ||||
| Attrition: cannot tell | 41-45 | 1.35 | 1.12 | ||||
| Overall: low | >45 | 1.38 | 1.12 | ||||
| Astolfi et al6,a | 1990-1998; Cohort study of nationwide sample from Italy; singleton, first born live births to mothers 20-29 y old and father >20 y old; n = 1,510,823 | Exposure: vital statistics dataset | Selection: none | 20-24 | 1.13 | ||
| Outcome: birth certificates | Exposure assessment: low | 25-29 | 1.00 | ||||
| Confounders adjusted: maternal age, infant sex, couple education, birth period | Outcome assessment: none | 30-34 | 1.03 | ||||
| Confounding factors: low | 35-39 | 1.12 | |||||
| Analytical: none | 40-44 | 1.23 | |||||
| Attrition: low | 45-49 | 1.16 | |||||
| Overall: low | ≥50 | 1.15 | |||||
| Basso and Wilcox7,a,b | 1995-2000; Cohort study of national sample from United States; married, non-Hispanic white primiparous women 20-34 y old | Exposure: birth certificate; why are the exposure and outcome the same? | Selection: low | 20-24 | 1.15 | ||
| Outcome: birth certificates | Exposure assessment: low | 25-29 | 1.00 | ||||
| Confounders adjusted: maternal education, smoking | Outcome assessment: none | 30-34 | 0.97 | ||||
| Confounding factors: low | 35-39 | 1.02 | |||||
| Analytical: none | 40-44 | 1.05 | |||||
| Attrition: low | 45-49 | 1.15 | |||||
| Overall: low | >50 | 0.97 | |||||
| Chen et al8,a | 1995-2000; Cohort study performed with nationwide data; 20-29 y-old nulliparous mother who had singleton live birth; n = 2,520,098 | Exposure: vital statistics dataset | Selection: none | <20 | 1.13 | 1.15 | 1.17 |
| Outcome: birth certificates | Exposure assessment: low | 20-29 | 1.00 | 1.00 | 1.00 | ||
| Confounders adjusted: race, maternal age, education, smoking, alcohol, infant sex, prenatal care | Outcome assessment: low | 30-34 | 1.00 | 0.98 | 1.03 | ||
| Confounding factors: none | 35-39 | 0.99 | 0.98 | 1.02 | |||
| Analytical: none | 40-44 | 0.96 | 0.99 | 1.02 | |||
| Attrition: low | 45-49 | 1.01 | 1.01 | 1.06 | |||
| Overall: low | ≥50 | 0.91 | 0.93 | 1.02 | |||
| Nahum and Stanislaw9,a | 1998-2000; Cohort study, private single clinic at Duke University; term, uncomplicated, singletons; n = 241 | Exposure: maternal history | Selection: low | Paternal age was not a significant predictor of birthweight if maternal age was specified (P = .08) | |||
| Outcome: charts | Exposure assessment: low | ||||||
| Confounders adjusted: none | Outcome assessment: none | ||||||
| Confounding factors: moderate | |||||||
| Analytical: low | |||||||
| Attrition: low | |||||||
| Overall: moderate | |||||||
| Olshan et al10,a | 1988-1991; Cohort study of statewide data from North Carolina; 20-34 y-old resident mothers who had singleton live birth; n = 254,892 | Exposure: birth files | Selection: low | <19 | 1.13 | 1.23 | 1.03 |
| Outcome: birth files | Exposure assessment: low | 20-24 | 1.04 | 1.09 | 0.98 | ||
| Confounders adjusted: maternal age, race, gravidity, smoking, marital status, education, infant sex | Outcome assessment: low | 25-29 | 1.00 | 1.00 | 1.00 | ||
| Confounding factors: none | 30-34 | 0.96 | 0.98 | 1.01 | |||
| Analytical: low | 35-39 | 0.96 | 1.03 | 0.95 | |||
| Attrition: low | 40-44 | 1.09 | 1.05 | 1.05 | |||
| Overall: low | 45-49 | 1.00 | 1.09 | 1.13 | |||
| >50 | 0.81 | 1.08 | 0.87 | ||||
| Reichman and Teitler11,a | 1998-2000; Cohort study of randomly selected births from 75 hospitals in the United States; >18 y-old mothers who had singleton live birth; n = 4621 | Exposure: history | Selection: moderate | <20 | 0.7 | ||
| Outcome: charts | Exposure assessment: low | 20-34 | 1.00 | ||||
| Confounders adjusted: maternal age, race, gravidity, marital status, socioeconomic status, infant sex | Outcome assessment: none | >34 | 1.7 | ||||
| Confounding factors: none | |||||||
| Analytical: low | |||||||
| Attrition: none | |||||||
| Overall: moderate | |||||||
| Selvin and Garfinkel12 | 1959-1967; Cohort study, singleton live births to white mothers in New York state (excluding New York City); n = 1,515,443 | Exposure: birth certificates | Selection: low | ≤19 | 8.58% | ||
| Outcome: birth certificates | Exposure assessment: low | 20-24 | 6.66% | ||||
| Confounder adjusted: maternal age | Outcome assessment: low | 25-29 | 5.77% | ||||
| Confounding factors: low | 30-34 | 5.63% | |||||
| Analytical: low | 35-39 | 6.08% | |||||
| Attrition: low | 40-44 | 6.57% | |||||
| Overall: low | 45-49 | 7.38% | |||||
| 50-54 | 7.82% | ||||||
| ≥55 | 7.99% | ||||||
| Total | 6.13% | ||||||
| Tough et al13,a | 1990-1996; Cohort study, provide wide data from Alberta, Canada; mothers between 25-29 y old; n = 259,903 | Exposure: birth certificates | Selection: none | ≤19 | 1.00 | 1.00 | |
| Outcome: birth certificates | Exposure assessment: low | 20-24 | 0.84 | 0.87 | |||
| Confounder adjusted: maternal age | Outcome assessment: none | 25-29 | 0.82 | 0.82 | |||
| Confounding factors: low | 30-34 | 0.77 | 0.77 | ||||
| Analytical: low | 35-39 | 0.76 | 0.75 | ||||
| Attrition: low | 40-44 | 0.79 | 0.81 | ||||
| Overall: low | 45-49 | 0.93 | 0.88 | ||||
| ≥50 | 0.98 | 0.96 | |||||
| Zhu et al14,a | 1980-1996; Cohort study; singleton live births in Danish fertility database; first child of couple; father <30 y old and >35 y old; n = 70,347 | Exposure: national database | Selection: low | 20-24 | 1.00 | ||
| Outcome: national database | Exposure assessment: low | 25-29 | 1.1 | ||||
| Confounders adjusted: maternal age, parity, education, income, infant sex, year of birth | Outcome assessment: low | 35-39 | 1.1 | ||||
| Confounding factors: none | 40-44 | 1.2 | |||||
| Analytical: low | 45-49 | 1.2 | |||||
| Attrition: none | ≥50 | 1.1 | |||||
| Overall: low | |||||||
aResults mentioned here are adjusted estimates; |
bData for preterm birth at <32 weeks' gestation. |
TABLE 2. Studies of paternal height and offspring birthweight
| Study | Study characteristics | Assessment | Risk of bias | Results | |
|---|---|---|---|---|---|
| Category, cm | Birthweight, ga | ||||
| Cawley et al15 | 1949-1950; Cohort study, singleton, live births and no neonatal death in 2 areas (Smethwick and Birmingham, UK); n = 1544 | Exposure: maternal history and measurement | Selection: low | <168 | 3239 |
| Outcome: charts | Exposure assessment: low | 168-173 | 3307 | ||
| Confounder adjusted: maternal height | Outcome assessment: none | 173-178 | 3325 | ||
| Confounding factors: moderate | 178-183 | 3329 | |||
| Analytical: low | >183 | 3447 | |||
| Attrition: moderate | |||||
| Overall: moderate | |||||
| Klebanoff25,b | 1959-1961; Cohort study, singleton, live births from single center in Copenhagen, Denmark; n = 3130 | Exposure: maternal history | Selection: low | ≤175 | 3325 |
| Outcome: charts | Exposure assessment: low | 175-178 | 3413 | ||
| Confounders adjusted: maternal birthweight, height, weight, smoking, hypertension, education, employment, infant sex, birth order | Outcome assessment: none | 179-182 | 3413 | ||
| Confounding factors: none | ≥183 | 3421 | |||
| Analytical: low | P for trend = .088 | ||||
| Attrition: moderate | |||||
| Overall: moderate | |||||
| Magnus et al17 | 1967-1979; Cohort study, singleton, live births who survived neonatal period; data from Norway birth registry; n = 3130 | Exposure: national database | Selection: moderate | Results reported as mean parental height in each 500-g birthweight category; not mean birthweight in each parental height group | |
| Outcome: national database | Exposure assessment: low | ||||
| Confounders adjusted: none | Outcome assessment: none | ||||
| Confounding factors: moderate | |||||
| Analytical: low | |||||
| Attrition: cannot tell | |||||
| Overall: moderate | |||||
| Miletic et al18 | 2002; Cohort study of all births in the county of Sibenik-Knin, Croatia; n = 550 | Exposure: survey in prenatal clinic | Selection: none | Paternal height correlated significantly with the neonate birthweight (P = .01) | |
| Outcome: hospital record | Exposure assessment: low | ||||
| Confounders adjusted: none | Outcome assessment: none | ||||
| Confounding factors: moderate | |||||
| Analytical: low | |||||
| Attrition: cannot tell | |||||
| Overall: moderate | |||||
| Morrison et al19 | 1980-1996; Cohort study, singleton, live births, term, without anomalies in Queensland University single center study; n = 8556 | Exposure: maternal history | Selection: low | Paternal height was significantly correlated with birthweight (P < .0007) | |
| Outcome: charts | Exposure assessment: low | ||||
| Confounder adjusted: maternal body mass index | Outcome assessment: none | ||||
| Confounding factors: moderate | |||||
| Analytical: low | |||||
| Attrition: cannot tell | |||||
| Overall: moderate | |||||
| Nahum and Stanislaw9,b | See Table 1 for details | Fathers with height >2 SD above and below the mean had 125-g difference in birthweight of index child | |||
| Pritchard et al20 | 1967-1971; Cohort study, singleton, live births in Aberdeen, UK, hospital and associated nursing homes of 32-43 weeks' gestational age; n = 5834 | Exposure: direct measurement | Selection: low | SD scores for birthweight were 0.29 higher (approximate correlation of 115-g birthweight) for taller men compared with shorter men | |
| Outcome: charts | Exposure assessment: moderate | ||||
| Confounder adjusted: maternal height | Outcome assessment: low | ||||
| Confounding factors: moderate | |||||
| Analytical: low | |||||
| Attrition: low | |||||
| Overall: moderate | |||||
| To et al21 | 1995-1996; Cohort study, singleton, live births of Chinese parents from single center in Hong Kong; >36 weeks' gestational age; n = 355 | Exposure: direct measurement | Selection: low | Paternal height divided in 5 strata (5 cm for 160-180 cm), significantly correlated with birthweight (P < .01) | |
| Outcome: charts | Exposure assessment: none | ||||
| Confounders adjusted: maternal prepregnancy weight and height | Outcome assessment: none | ||||
| Confounding factors: low | |||||
| Analytical: low | |||||
| Attrition: moderate | |||||
| Overall: moderate | |||||
| Wilcox et al22,b | 1992-1993; Cohort study, singleton, term, live births without congenital anomaly from single center in Nottingham, UK; n = 571 | Exposure: direct measurement | Selection: low | <170 | 3322 |
| Outcome: charts | Exposure assessment: none | 170-174 | 3406 | ||
| Confounders adjusted: smoking, maternal height, paternal weight | Outcome assessment: none | 175-179 | 3465 | ||
| Confounding factors: low | 180-184 | 3474 | |||
| Analytical: low | 185-189 | 3503 | |||
| Attrition: low | >190 | 3585 | |||
| Overall: low | |||||
| Winikoff and Debrovner23 | 1992-1993; Cohort study, singleton primiparous, term live births; uncomplicated pregnancies from a single clinic in New York; n = 259 | Exposure: maternal history | Selection: moderate | Paternal height was significantly associated with variations in birthweight (P < .05) | |
| Outcome: charts | Exposure assessment: low | ||||
| Confounders adjusted: maternal height, paternal weight, maternal prepregnancy weight, weight gain during pregnancy | Outcome assessment: none | ||||
| Confounding factors: low | |||||
| Analytical: low | |||||
| Attrition: cannot tell | |||||
| Overall: moderate | |||||
aData are given as mean ± SD; |
bResults mentioned here are adjusted estimates. |
TABLE 3. Studies of paternal weight and body mass index and their relation to birthweight and low birthweight
| Study | Study characteristics, assessment and risk of biases | Results | |
|---|---|---|---|
| Category | Birthweight, ga | ||
| Klebanoff25,b | See Table 2 for details | <20.08 kg/m2 | 3188 |
| 20.08-21.56 kg/m2 | 3276 | ||
| 21.57-23.05 kg/m2 | 3261 | ||
| >23.05 kg/m2 | 3293 (P for trend = .049) | ||
| Magnus et al17 | See Table 2 for details | Results reported as mean parental weight in each 500-g birthweight category; not mean birthweight in each parental weight group | |
| Miletic et al18 | See Table 2 for details | Paternal bodyweight correlated significantly with the neonate birthweight (P = .01) | |
| Morrison et al19 | See Table 2 for details | Paternal weight was not significantly correlated with birthweight (P > .05) | |
| Nahum and Stanislaw9,b | See Table 1 for details | Paternal weight and BMI were not significant predictor of birthweight once maternal weight (P = .16) and BMI (P = .42) were taken in account, respectively | |
| To et al21 | See Table 2 for details | Paternal weight divided in 9 strata (5 kg strata for <50 to >90 kg) was not correlated with birthweight (P = .052); paternal BMI divided in 4 strata (5 kg/m2 strata for <20 to >35 kg/m2) was not correlated with birthweight (P = .33) | |
| Wilcox et al22,b | See Table 2 for details | <59 kg | 3522 |
| 60-69 kg | 3320 | ||
| 70-79 kg | 3486 | ||
| 80-89 kg | 3511 | ||
| 90-99 kg | 3550 | ||
| 100-109 kg | 3657 | ||
| >110 kg | 3608 | ||
| Winikoff and Debrovner23 | See Table 2 for details | Paternal weight was not associated with variations in birthweight (P > .05) | |
aData are given as mean ± SD; |
bResults mentioned here are adjusted estimates. |
TABLE 4. Paternal birthweight and relation to birthweight, low birthweight, and preterm births
| Author | Study characteristics | Assessment | Risk of bias | Results | ||
|---|---|---|---|---|---|---|
| Category | Birthweight | Preterm birth | ||||
| Coutinho et al24 | 1989-91; Cohort study of fathers born from 1956-1975 derived from Illinois vital records; n = 128,152 | Exposure: birth record | Selection: low | Black father LBW | Infant LBW, 14.3%; RR 1.3 (95% CI, 1.1–1.5) | |
| Outcome: birth certificate | Exposure assessment: low | Black father normal birthweight | Infant LBW, 11.5% | |||
| Confounders adjusted: none | Outcome assessment: low | White father LBW | Infant LBW, 5.7%; RR 1.2 (95% CI, 1.0–1.2) | |||
| Confounding factors: moderate | White father normal birthweight | Infant LBW, 5.0% | ||||
| Analytical: low | ||||||
| Attrition: cannot tell | ||||||
| Overall: moderate | ||||||
| Klebanoff et al16 | 1959-1961; Cohort study, fathers born in this period derived from Danish population register and their singleton, liveborn, children born from 1974-1989; n = 1258 | Exposure: birth record | Selection: low | <3 kg | 5.1% | |
| Outcome: birth certificate | Exposure assessment: moderate | 3-3.9 kg | 7.1% | |||
| Confounders adjusted: maternal birthweight | Outcome assessment: low | >4 kg | 6.9% | |||
| Confounding factors: moderate | ||||||
| Analytical: low | ||||||
| Attrition: moderate | ||||||
| Overall: moderate | ||||||
| Klebanoff25,a | See Table 2 for details | <3 kg | 3317 g | |||
| 3-3.9 kg | 3384 g | |||||
| >4 kg | 3493 g | |||||
| P for trend = .002 | ||||||
| Little26 | 12-mo period; matched cohort study based on alcohol drinking status, singleton, live births from single center in Copenhagen, Denmark; n = 377 | Exposure: maternal history | Selection: low | <3 kg | 3487 g | |
| Outcome: maternal history | Exposure assessment: low | 3-3.999 kg | 3555 g | |||
| Confounders adjusted: maternal birthweight | Outcome assessment: none | >4 kg | 3707 g | |||
| Confounding factors: moderate | ||||||
| Analytical: low | ||||||
| Attrition: moderate | ||||||
| Overall: moderate | ||||||
| Magnus et al27 | 1967-1998; Cohort study, singleton, live births from medical birth registry of Norway; n = 3130 | Exposure: birth register | Selection: low | Father normal birthweight | Infant LBW, 2.9% | |
| Outcome: birth register | Exposure assessment: low | Father LBW | Infant LBW, 6.8% | |||
| Confounders adjusted: none | Outcome assessment: low | |||||
| Confounding factors: moderate | ||||||
| Analytical: none | ||||||
| Attrition: cannot tell | ||||||
| Overall: moderate | ||||||
aResults mentioned here are adjusted estimates. |
TABLE 5. Studies of paternal occupation and low birthweight, preterm, and small-for-gestational-age births
| Author | Study characteristics | Exposure and its assessment | Assessment | Risk of bias | Results | |||
|---|---|---|---|---|---|---|---|---|
| Category | LBW, OR (95% CI) | PTB, OR (95% CI) | SGA, OR (95% CI) | |||||
| Dimich-Ward et al28,a | 1952-1988; Cohort study; fathers who worked in saw mills for at least 1 y in British Columbia, Canada; n = 2128 | Chlorophenate wood preservative assessed by calculating exposure time from type of job | Outcome: birth certificate | Selection: low | Up to 3 mo before conception | 0.99 | 1.00 | 1.00 |
| Confounders adjusted: maternal and paternal age, infant sex, birth year | Exposure assessment: moderate | 3 mo before conception | 1.01 | 0.99 | 1.00 | |||
| Outcome assessment: low | Through entire pregnancy | 0.99 | 0.96 | 1.01 | ||||
| Confounding factors: low | ||||||||
| Analytical: low | ||||||||
| Attrition: cannot tell | ||||||||
| Overall: moderate | ||||||||
| Hooiveld et al29,a | 2001; Comparative cohort study; fathers who worked as painters (472 cases) were compared with carpenters (462 control subjects) in The Netherlands; n = 934 | Organic solvents for painters assessed by questionnaire | Outcome: questionnaire | Selection: low | Low level (0.17–0.38) | 1.5 | 1.6 | |
| Confounders adjusted: maternal age, smoking, alcohol use, chemical exposure; paternal smoking, alcohol use | Exposure assessment: moderate | Intermediate level (0.38–1.02) | 1.6 | 1.5 | ||||
| Outcome assessment: low | High level (1.03–4.66) | 1.9 | 0.8 | |||||
| Confounding factors: none | ||||||||
| Analytical: none | ||||||||
| Attrition: moderate | ||||||||
| Overall: moderate | ||||||||
| Kristensen et al30,a | Male printing workers between 1930-1974 alive at 1960 census; exposure to lead, solvent, and both combined; n = 6251 | Lead and solvent exposure classified based on job codes | Outcome: national birth register | Selection: low | Lead only | 0.9 | 1.2 | |
| Confounders adjusted: gestational age, birth order, infant sex, multiple gestation, previous still birth, consanguinity, maternal chronic diseases | Exposure assessment: moderate | Solvents only | 1.1 | 1.4 | ||||
| Outcome assessment: none | Lead plus solvent | 1.2 | 1.2 | |||||
| Confounding factors: none | Other | 1.0 | 1.0 | |||||
| Analytical: low | ||||||||
| Attrition: Cannot tell | ||||||||
| Overall: moderate | ||||||||
| Lawson et al31,a | 1987-1988; Matched cohort study; workers from plants in New York and Missouri; matched population selected from neighbors; n = 1153 | 2,3,7,8-Tetrachloro-dibenzo-p-dioxin assessed from blood sample and modeled calculation | Outcome: birth certificate or maternal report | Selection: low | Reference | Mean birthweight, 3402 g | 0.8 | |
| Confounders adjusted: maternal age, accidents, smoking, alcohol and medication use | Exposure assessment: moderate | <20 pg/g | Mean birthweight, 3396 g | |||||
| Outcome assessment: low | 20-254 pg/g | Mean birthweight, 3360 g | ||||||
| Confounding factors: moderate | >255 pg/g | Mean birthweight, 3485 g | ||||||
| Analytical: low | ||||||||
| Attrition: moderate | ||||||||
| Overall: moderate | ||||||||
| Lin et al32,a | 1981-1992; Matched cohort study; fathers exposed to high lead levels (>40 μg/dL before 1986 and >25 μg/dL after 1986 (n = 747) compared with male bus drivers (n = 2259) in New York, 1974-1989 (n = 1258) | Lead exposure assessed from laboratory reports of workers | Outcome: birth certificate | Selection: low | General exposure (risk ratio) | 1.00 | 0.89 | 0.86 |
| Confounders adjusted: paternal age, maternal education, maternal complications, prenatal care, race, parity, infant sex | Exposure assessment: low | Lead exposure for >5 years (risk ratio) | 3.40 | 3.03 | 0.82 | |||
| Outcome assessment: none | ||||||||
| Confounding factors: none | ||||||||
| Analytical: low | ||||||||
| Attrition: cannot tell | ||||||||
| Overall: low | ||||||||
| Michalek et al33 | 1961-1971; Matched cohort study; children of fathers exposed to herbicide spray during Vietnam conflict (n = 859) compared with children of unexposed Air Force veterans (n = 1223); n = 2082 | 2,3,7,8-Tetrachloro-dibenzo-p-dioxin assessed from blood sample and modeled calculation | Outcome: charts | Selection: low | Control (≤10 ppt) | 1.0 | 1.0 | |
| Confounders adjusted: none | Exposure assessment: moderate | Cases (≤10 ppt) | 1.4 | 0.9 | ||||
| Outcome assessment: none | Low (<79 ppt) | 0.5 | 0.9 | |||||
| Confounding factors: moderate | High (≥79 ppt) | 1.3 | 0.9 | |||||
| Analytical: low | ||||||||
| Attrition: moderate | ||||||||
| Overall: moderate | ||||||||
| Milham and Ossiander34 | 1980-2002; Cohort study; fathers who were flour mill workers in Washington state; n = 59 | Fumigants used to kill insects, mainly methyl bromide and phosphine; assessed by history of work-related exposure | Outcome: birth certificate | Selection: low | Unexposed (male children) | Mean birthweight, 3511 g | ||
| Confounders adjusted: none | Exposure assessment: moderate | Unexposed (female children) | Mean birthweight, 3389 g | |||||
| Outcome assessment: none | Exposed (male children) | Mean birthweight, 3180 g | ||||||
| Confounding factors: moderate | Exposed (female children) | Mean birthweight, 3602 g | ||||||
| Analytical: moderate | ||||||||
| Attrition: cannot tell | ||||||||
| Overall: moderate | ||||||||
| Min et al35 | 1981-1989; Case control study; control subjects enrolled in another study in Baltimore-Washington DC; cases (n = 220) were LBW; controls were not LBW (n = 522); n = 742 | Lead exposure assessed by history regarding type of job and hours exposed | Outcome: birth certificate | Selection: low | No exposure | 1.0 | ||
| Confounders adjusted: none | Exposure assessment: low | Threshold, ≤0.01 | 0.70 | |||||
| Outcome assessment: none | Threshold, >0.1 to <0.5 | 1.67 | ||||||
| Confounding factors: moderate | Threshold, ≥0.5 | 4.7 | ||||||
| Analytical: moderate | ||||||||
| Attrition: low | ||||||||
| Overall: moderate | ||||||||
| Mjoen et al36,a | 1976-1995; Cohort study; all births in national registry of Norway where exposure risk can be determined; n = 28,435 | Radiofrequency fields exposure assessed based on type of occupation | Outcome: birth certificate | Selection: low | Probably unexposed | 1.00 | 1.00 | |
| Confounders adjusted: calendar year, place of birth, education | Exposure assessment: moderate | Possibly exposed | 0.99 | 1.03 | ||||
| Outcome assessment: none | Probably exposed | 1.08 | 1.03 | |||||
| Confounding factors: low | ||||||||
| Analytical: none | ||||||||
| Attrition: cannot tell | ||||||||
| Overall: moderate | ||||||||
| Sanjose et al37 | 1981-1984; Cohort study in Scotland, regarding parental occupation and liveborn infants; n = 177,746 | Classified as manual and nonmanual jobs; no direct assessment of any exposure | Outcome: birth certificate | Selection: none | Nonmanual | 3.8% | 3.9% | 3.4% |
| Confounders adjusted: none | Exposure assessment: moderate | Manual; potential hazard | 5.1% | 4.5% | 4.7% | |||
| Outcome assessment: none | Manual; other | 6.0% | 5.2% | 5.6% | ||||
| Confounding factors: moderate | ||||||||
| Analytical: none | ||||||||
| Attrition: cannot tell | ||||||||
| Overall: moderate | ||||||||
| Savitz et al38,a,c | 1980; Cohort study; “National Natality Study” in United States; n = 177,746 | Paternal occupations held within 12 mo of birth | Outcome: birth certificate | Selection: low | X-ray | 1.5 | ||
| Confounders adjusted: maternal smoking, race, infant sex | Exposure assessment: moderate | Benzene | 1.5 | |||||
| Outcome assessment: none | Chromium | 1.4 | ||||||
| Confounding factors: low | Minerals and compounds | 1.3 | ||||||
| Analytical: none | ||||||||
| Attrition: cannot tell | ||||||||
| Overall: moderate | ||||||||
aResults mentioned here are adjusted estimates; |
bOnly data which were significant are reported here; |
cOnly significant results are reported; all other occupations had nonsignificant relationships. |
TABLE 6. Miscellaneous paternal factors and low birthweight, preterm, and small-for-gestational-age births
| Study | Study characteristics | Assessment | Risk of bias | Results | |||
|---|---|---|---|---|---|---|---|
| Category | LBW, OR (95% CI) | PTB, OR (95% CI) | SGA, OR (95% CI) | ||||
| PATERNAL EDUCATION | |||||||
| Abel et al5,a | See Table 1 for details | Less than high school | 9.3% male; 8.4% female | ||||
| High school | 5.5% male; 7.8% female | ||||||
| College | 6.3% male; 5.5% female | ||||||
| Parker and Schoendorf39 | 1984-1988; Cohort study; natality data from 47 states; singleton live births to married white or black women >17 y old; n = 9,740,852 | Exposure: national database | Selection: low | Less than high school | 1.53 | ||
| Outcome: national database | Exposure assessment: moderate | High school graduate | 1.28 | ||||
| Confounders adjusted: maternal race, age, parity, education | Outcome assessment: none | Some college | 1.14 | ||||
| Confounding factors: low | College graduate | 1.00 | |||||
| Analytical: none | |||||||
| Attrition: low | |||||||
| Overall: moderate | |||||||
| PATERNAL ALCOHOL USE | |||||||
| Little26 | See Table 4 for details | Occasional | Mean birthweight, 3646 g | Mean gestational age, 41.2 wk | |||
| Regular | Mean birthweight, 3465 g | Mean gestational age, 40.5 wk | |||||
| Passaro et al40 | 1991-1992; Cohort study; Avon County, England; singleton live births; n = 7756 | Exposure: questionnaire | Selection: none | ||||
| Outcome: hospital records | Exposure assessment: none | None | 5.6% | 6.4% | NA | ||
| Confounders adjusted: gestational age, infant sex, primiparity, maternal smoking, maternal body mass index, maternal race, maternal education, maternal age, marital status, marijuana use, caffeine use, alcohol intake | Outcome assessment: none | Less than weekly | 4.1% | 5.7% | |||
| Confounding factors: none | Weekly | 3.5% | 5.4% | ||||
| Analytical: none | 1-2 drinks/d | 4.4% | 5.9% | ||||
| Attrition: moderate | 3+ drinks/d | 4.3% | 6.5% | ||||
| Overall: moderate | |||||||
| Savitz et al41 | 1959-1966; Cohort study, San Francisco, CA; singleton live births to married women; n = 10,232 | Exposure: history | Selection: low | No alcohol | 1.0 | 1.0 | |
| Outcome: charts | Exposure assessment: low | 0-0.5 drinks/d | 0.9 | 1.0 | |||
| Confounders adjusted: parental smoking, maternal alcohol use, race, education, prenatal care, infant sex | Outcome assessment: none | 0.5-1 drinks/d | 1.1 | 1.0 | |||
| Confounding factors: low | 1-1.5 drinks/d | 0.8 | 1.2 | ||||
| Analytical: low | 1.5-2 drinks/d | 1.0 | 0.9 | ||||
| Attrition: moderate | >2 drinks/d | 0.8 | 1.1 | ||||
| Overall: moderate | |||||||
| Windham et al42 | 1986-1987; Control arm of a case-control study, California; singleton live births; n = 1252 | Exposure: interview | Selection: none | No alcohol | 7.3% | 14.8% | 8.0%; AOR, 1.0 (Reference) |
| Outcome: birth certificate | Exposure assessment: none | 1-13 drinks/wk | 7.1% | 14.0% | 9.3%; AOR, 1.2 (0.7–1.9) | ||
| Confounders adjusted: maternal age, race, parity, marital status, education, employment status, insurance status, caffeine consumption, cigarette smoking, hypertension, infant sex | Outcome assessment: none | 14-20 drinks/wk | 2.7% | 10.8% | 13.5%; AOR, 1.3 (0.5–2.9) | ||
| Confounding factors: none | ≥21 drinks/wk | 9.6% | 17.8% | 16.4%; AOR, 1.4 (0.7–1.9) | |||
| Analytical: low | |||||||
| Attrition: none | |||||||
| Overall: moderate | |||||||
aResults mentioned here are adjusted estimates. |
Paternal age
There was variability in age cut-offs that were used in the studies as well as the reference age for comparison of groups. Exploratory analysis of a relationship between paternal age and LBW births was conducted. Figure 2 demonstrates the relationship of paternal age (mid values from all reported age groups and conversion of the 25- to 28-year age group as the reference group for each study) and LBW births in 6 studies that reported the odds of LBW births in various age groups. A “saucer-shaped” association can be inferred with higher odds at both extremes. No association between paternal age and PTB or SGA births was identified in any of the studies. Characteristics of the included studies, assessment of biases, and reported results are outlined in Table 1.

FIGURE 2.
Scatter plot of paternal age and odds ratio for low birthweight (LBW) births that were reported in various age groups.
Shah. Paternal factors and LBW/PTB. Am J Obstet Gynecol 2010.
Paternal height
Paternal height showed significant correlation with birthweight of the offspring in most of the studies. On average, there was 125-150 g reduction in birthweight of the offspring of short vs tall fathers. Characteristics of the included studies, assessment of biases, and reported results are given in Table 2.
Paternal weight and body mass
Most of the studies reported a nonsignificant relationship with paternal body weight or mass and birthweight and LBW births. In 1 study, a significant relationship became nonsignificant when maternal body mass was considered. Characteristics of the included studies, assessment of biases, and reported results are given in Table 3.
Paternal birthweight
Three studies reported that an infant's birthweight increased as paternal birthweight increased. The odds of a LBW birth were higher if the father had a LBW birth. Interestingly, 1 study reported higher rates of PTBs as the father's birthweight increased; however, this might be attributed to maternal characteristic. Characteristics of the included studies, assessment of biases, and reported results are given in Table 4.
Paternal occupation
Higher and prolonged lead exposures were associated with higher risk of LBW birth and PTB; however, details of timing of exposure in relation to pregnancy were not available in detail to assess direct effect. One large study reported a higher adjusted risk of SGA births among workers who were exposed to benzene, chromium, and other minerals and a higher risk of PTBs among workers who were exposed to x-rays. Other occupations that were assessed were not associated with higher risk of adverse outcomes. Characteristics of the included studies, assessment of biases, and reported results are given in Table 5.
Paternal education
One study reported a higher risk of LBW births and another reported a higher risk of PTBs among fathers who had a high school education only, compared with fathers who had a college education. Characteristics of the included studies, assessment of biases, and reported results are given in Table 6.
Paternal alcohol use
One small study reported a 200-g reduction in birthweight with regular alcohol use; other studies reported no difference in the risk of LBW birth or PTBs with different levels of paternal alcohol use.26, 40, 41, 42 Characteristics of the included studies, assessment of biases, and reported results are given in Table 6.
Comment
In this systematic review of 36 studies on paternal factors and birth outcomes, certain positive and negative associations were observed. Extreme paternal ages (<20 and >40 years) may be associated with LBW; however, no consistent associations with PTBs and SGA births were identified. Paternal height and paternal occupational exposure to lead were associated with LBW and birthweight of the offspring. The infant's birthweight increased with a higher paternal birthweight. Paternal weight, body mass, and occupational exposures to herbicides, plant work, woodwork and paternal alcohol use were not associated with birth outcomes. A lower level of paternal education was associated with LBW/PTB and SGA births; however, confirmation of data from larger studies is warranted.
Paternal age
Advanced paternal age has been linked with fetal loss,54 congenital malformations,55 single gene disorders,56 lower intelligence, dyslexia,57 and mental disorders58 in children. Studies of the impact of paternal age on LBW, PTB, or SGA outcomes have concluded varied results.5, 6, 10, 14 Biologic rationale behind the influence of paternal age on birth outcomes stems from the identification of greater expression of paternal genes on the placenta59 and higher chances of mutation that involves those genes in immature men compared with mature men60 and in men of advanced age.61 A paternal “weathering” phenomenon (ie, biologic effects of male aging that is hastened by harsh living conditions over years) has been suspected.11 The overall impression from our systematic review of included studies and the plot of paternal age–LBW birth incidence curve suggest that, if there was an effect of paternal age on LBW birth, it would appear to be modest for advanced paternal age.
Paternal anthropometry
All 10 reviewed studies reported an increase in birthweight as father's height increased. The magnitude of increase between the lowest group and the highest group was approximately 125-150 g. No studies reported incidences of LBW, PTB, or SGA births. The effect is presumed to be of genetic origin.21 Studies of paternal weight and its influence on birthweight revealed contradictory results. Two studies reported an approximate 75- to 100-g increase in birthweight among the highest weight/body mass index group,22, 25 compared with the lowest weight/body mass index group. Three studies reported no significant influence.9, 19, 21 All of these studies had very small sample sizes, and a large population-based study is warranted.
Paternal birthweight
Lower paternal birthweight was associated with lower infant birthweight. Paternal LBW was associated with higher risk of an infant with LBW, which is an effect that is similar to maternal LBW. PTB rate was lower for fathers in the LBW birth category. However, this information comes from very few and small studies. Ascertainment issues regarding birthweight of the father should not be ignored in the interpretation of these results. Also, studies from different countries were included in this review; therefore, it may have affected the results because there are different norms for birthweight in different ethnic backgrounds.
Paternal occupational exposure
There are 2 pathways by which paternal exposure contribute to an effect on birth outcomes: either paternal exposure leads to maternal exposure and the effect is exerted or paternal exposure leads to alteration in the germ cell line that leads to either increased infertility or abnormality in conception.3 Lead, dioxin, and organic solvents are the more commonly studied exposures. Animal experiments reported lower birthweight after male animal exposure to lead.62 Lead exposure has been shown to be associated with infertility, still births, and spontaneous abortions.38 The effect is suspected to be due to effects on the metabolic activity of the sperm.63 Higher and prolonged exposure to lead may be associated with increased risk of LBW births and PTBs; however, ascertainment bias played a major role in included studies. Agent Orange was a widely used herbicide in Vietnam, and contamination of this by dioxin prompted a series of studies that explored the association of paternal exposure with birth outcomes.31 Two studies reported no significant association between exposure to dioxin and LBW birth or PTB.31, 33 Organic solvents can pass the blood-testis barrier and the placenta. Two studies of this association revealed no significant association.29, 30 Several studies of occupational exposure assessment have classified exposure based on interviews, databases, and expected hours of exposure.28, 29, 30, 31, 34 The possibility of misclassification and recall bias cannot be ruled out.
Other paternal factors
Paternal alcohol intake was not associated significantly with PTB/SGA births in 1 study,41 but another study reported a 180-g increase in mean birthweight among offspring of the occasional drinker, compared with regular drinkers.48 The biologic rationale for such an effect remains to be understood. Less than a high school education was associated with a higher rate of PTB, and education less than college level was associated with higher odds of LBW births. Paternal low education level may be a marker for other underlying health determinants such as poverty, adverse home environment, and associated stress.
There was significant heterogeneity in the reported studies that assessed paternal factors and its association to offspring outcomes. Keeping this in mind, we planned for a systematic review from the onset and not metaanalyses. Major clinical heterogeneities among studies were identified for inclusion of the studies (single institution-based study vs national sample) and for adjustment of confounders (different studies controlled for different confounders). A number of studies identified associations in univariate analyses; however, when confounders such as maternal factors were considered, the association became nonsignificant. The major issues with parental occupational exposure were ascertainment of a bias for exposure and recall bias.
Strengths of this systematic review lie in the focused question, comprehensive and extensive literature search, and inclusion of studies from various countries. However, there are limitations of this review. First, there was heterogeneity in studies even within various exposure categories. Second, data on paternal factors are not collected regularly because fathers may not be present at prenatal visits and data are collected from mothers. The information that is collected could be subject to inaccuracies. Additionally, occupational exposure data were obtained from administrative databases or calculated in terms of duration or intensity of exposure. This is subject to ascertainment bias. Additionally, no detailed information regarding the timing of exposure and the protection used by fathers were reported. Third, various studies adjusted for different confounders in their analyses, and some studies did not adjust for confounders. It is important to adjust for various maternal confounders to assess the independent effect of paternal exposure. This limited our ability to conclude anything definitively about any of the factors. Fourth, publication bias should be considered. There is a possibility that, if the studies reported no association for any of the paternal exposures, there may have been less likelihood of publication. Fifth, we restricted our search to English language publications primarily because of the scope of information that may or may not be available in other languages. Literature searchers have found minimal difference with the inclusion of non-English language articles.64 We have not included gray literature, abstracts, and proceedings because the quality of such studies cannot be assessed adequately. Finally, none of the studies used any objective measure to confirm paternity; the data on paternity were obtained from maternal history in all studies.
Implications
There are clinically significant and important implications of these results. Pregnancies that were conceived from younger and advanced age fathers, short-statured fathers, fathers who were LBW at birth, and fathers with less than a college education could be considered to be at a greater risk. This information can be used during counseling and education sessions.
Conclusion
In this comprehensive systematic review of paternal factors, associations were identified for paternal age, height, and LBW. Higher paternal birthweight resulted in heavier offspring. Heavy and prolonged lead exposure may be associated with LBW. Paternal weight, body mass, and workers with occupational exposures to herbicides, plant work, and wood were not associated with birth outcomes. Low paternal education may be associated with LBW/PTB births; however, further studies are warranted.
Acknowledgments
We sincerely thank Elizabeth Uleryk, Chief Librarian at the Hospital for Sick Children, Toronto, for her contribution in developing search strategy and running searches on a periodic basis, for which she did not receive any compensation. Contributors: guarantor: Shah PS; grant concept and design: all members of the group; study concept and design: Shah PS; acquisition of data, analysis, and interpretation of data, drafting of the manuscript: Shah PS; critical revision of the manuscript for intellectual content: Shah PS and all members of group. Members of the Knowledge Synthesis Group on determinants of LBW/preterm births: Prakesh S Shah, University of Toronto, Toronto, Ontario, Canada; Arne Ohlsson, University of Toronto, Ontario, Canada; Sarah D McDonald, McMaster University, Hamilton, Ontario, Canada; Eileen Hutton, McMaster University, Hamilton, Ontario, Canada; Vibhuti Shah, University of Toronto, Toronto, Ontario, Canada; Joseph Beyene, University of Toronto, Toronto, Ontario, Canada; Corine Frick, University of Calgary, Calgary, Alberta, Canada; Fran Scott, University of Toronto, Toronto, Ontario, Canada; Kellie E Murphy, University of Toronto, Ontario, Canada; Christine Newburn-Cook, University of Alberta, Edmonton, Alberta, Canada; Victoria Allen, Dalhousie University, Halifax, Nova Scotia, Canada.
Appendix
Quality assessment tool
| Bias | None | Low | Moderate | High | Cannot tell |
|---|---|---|---|---|---|
| Selection | Consecutive unselected population | Sample selected from large population; selection criteria not defined | Sample selection ambiguous; sample may be representative | Sample selection ambiguous; sample likely not representative | NA |
| Sample selected from general population rather than a select group | A select group of population (eg, based on race, ethnicity, residence) | Eligibility criteria not explained | A very select population was studied, which made it difficult to generalize findings | NA | |
| Rationale for case and control selection explained | Rationale for case and control subjects not explained | NA | |||
| Follow-up or assessment time explained | Follow-up or assessment time not explained | NA | |||
| Exposure assessment | Direct questioning (interview) or completion of survey by mother at the time of exposure or close to the time of exposure | Assessment of exposure from global dataset | Extrapolating data from population exposure sample (with some assumptions) and not direct assessment at any time | Indirect method of assessment (obtaining data from others and not from mother or father) | NA |
| Direct measurement of exposure (laboratory) | Indirect assessment (postal survey, mailed questionnaire) | NA | |||
| Outcome assessment | Assessment from hospital record, birth certificate, or direct question to mother regarding birthweight | Assessment from administrative database | Assessment from “open-ended” questions (was your baby early? or premature? or small? or before due date) | Assessment from nonvalidated sources or generic estimate from overall population | NA |
| Direct question to mother regarding gestational age | NA | ||||
| Confounding factor | Controlled for common confounders | Only certain confounders adjusted | Not controlled for confounders | NA | |
| Analytical | Analyses appropriate for the type of sample | Analyses not accounting for common statistical adjustment (eg, multiple analyses) when appropriate | Sample size estimation unclear, or only subsample of eligible patients was studied | Analyses inappropriate for the type of sample/study | NA |
| Analytical method accounted for sampling strategy in cross-sectional study | Sample size calculation not performed; all available eligible patients studied | NA | |||
| Sample size calculation performed and adequate sample studied | Sample size calculated; reasons for not meeting sample size given | NA | |||
| Attrition | 0-10% attrition and reasons for loss of follow-up data explained | 0-10% attrition and reasons for loss of follow-up data not explained | 11-20% attrition; reasons for loss of follow-up data not explained | >20% attrition; reasons for loss of follow-up data not explained | NA |
| All subjects from initiation of study to the final outcome assessment were accounted for | 11-20% attrition; reasons for loss of follow-up data explained | >20% attrition but reasons for loss of follow up explained | NA | ||
| All subjects from initiation of study to final outcome assessment not accounted for | NA |
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This study was supported by funding from the Canadian Institute of Health Research (CIHR) Knowledge Synthesis/Translation Grant no. KRS 86242. The CIHR has played no role in the analyses, the writing of the report, the interpretation of data, or the decision to submit the manuscript.
PII: S0002-9378(09)00952-1
doi:10.1016/j.ajog.2009.08.026
© 2010 Mosby, Inc. All rights reserved.
Refers to article:
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Do fathers matter? Paternal contributions to birth outcomes and racial disparities
Volume 202, Issue 2 , Pages 103-123, February 2010

