Paternal Occupational Exposure Research Articles

Birth defects among offspring of California firefighters, 2007–2019

PurposeLimited research examines birth defects from maternal or paternal firefighting exposure. This study aims to assess if maternal or paternal occupational exposure to firefighting during periconception is associated with offspring birth defects. MethodsData from California birth certificates (2007–2019) were linked to maternal / offspring hospitalization records. Occupation during the periconceptional period was categorized from vital statistics as the following: paternal non-firefighting (n = 4,135,849), paternal firefighting (n = 22,732), maternal non-firefighting (n = 3,332,255) and maternal firefighting (n = 502). Birth defects were identified using ICD codes, grouped by anatomical regions. Adjusted odds ratios were estimated, and sensitivity analyses explored police officer reference groups and detailed birth defect categories. ResultsOffspring of paternal firefighters had lower odds of circulatory defects (aOR = 0.9, 95% CI 0.8, 1.0), oral clefts (aOR = 0.6, 95% CI 0.4, 0.8) and respiratory defects (0.7, 95% CI 0.6, 0.9) compared to paternal non-firefighters. Associations between maternal firefighting and offspring birth defects were imprecise. Substituting police officers as the reference group attenuated findings. ConclusionsOffspring of paternal firefighters may have similar or slightly lower birth defect odds compared to offspring of non-firefighters. Limited data was available for assessing maternal firefighting outcomes. Future studies should prioritize studies using occupational exposure matrices to limit misclassification of exposure.

P-584 Occupational paternal risk factors for cryptorchidism and hypospadias in the offspring: a case-control study

Abstract Study question Does paternal occupational exposures to reprotoxic chemical and physical hazards constitute risk factors to cryptorchidism and hypospadias in the offspring? Summary answer Paternal occupational reprotoxic exposures, determined through a job exposure matrix, and paternal rural lifestyle are associated with cryptorchidism, hypospadias, and other genital congenital malformations. What is known already Cryptorchidism and hypospadias are the most common congenital malformations of the male urogenital organs. Over the past century, these congenital malformations, which are associated with testicular cancer and impaired semen quality, have been included into a common disease spectrum known as the testicular dysgenesis syndrome. The association between urogenital congenital malformations and fetal exposure to many factors has been suggested, in particular to genetic and epigenetic factors and environmental factors. There is growing scientific evidence that both maternal and paternal exposure at the time of fertilization play a role after fertilization. Study design, size, duration This is a case-control study with standardized data collection of a 220 father-child cohort recruited from the consultants of our genetic counseling service at the medical university of Sfax (Tunisia), over two years. Participants/materials, setting, methods We compared 110 children diagnosed with congenital malformations to 110 children without any congenital defects. Controls did not differ from the total cohort in confounding variables. Information about paternal jobs held early in pregnancy was collected. Determined via a job exposure matrix, paternal occupational reprotoxic exposures were assessed. Logistic regression analysis was performed to assess the associations between paternal occupational exposures and the congenital testicular dysgenesis syndrome in offspring, including cryptorchidism and hypospadias. Main results and the role of chance 75.54% of children had congenital heart defects and 24.54% of them had genital malformations (n = 27). Paternal occupational exposures to pesticides were associated with the risk of developing birth defects (odds ratio = 17.568 (95% CI), 2.258-136.673). Our results indicate that paternal exposure to pesticides, phthalates, alkylphenolic compounds and other endocrine disruptors was associated with genital and cardiac birth defects. Both cryptorchidism and hypospadias in offspring were associated with paternal rural lifestyle as well as the absence of a maternal job. Limitations, reasons for caution The cohort size in this case-control study may limit the statistical power of the logistical regression to detect associations. Additionally, cases and controls may be selected in a way that does not represent the general population accurately. This can introduce bias and affect the external validity of the study. Wider implications of the findings Including paternal exposures in subsequent investigations of risk factors for cryptorchidism and hypospadias, and further exploring the connection between paternal pesticide exposure and epigenetic alterations, may offer insights into their impact on paternal spermatogenesis, sperm small RNAs, and the potential development of congenital testicular dysgenesis syndrome in future generations. Trial registration number 0400/2022

P-010 Impact of paternal occupational exposures on fetal loss in the female partner: a systematic review

Abstract Study question Are paternal occupational exposures associated with a higher risk of fetal loss in the unexposed female partner? Summary answer Significant positive associations between paternal occupational exposures and fetal loss were retrieved, for chemical and physical agents and for several occupations. What is known already Adverse pregnancy outcomes are frequent and, in its recently updated guidelines, the ESHRE reinforced the interest of exploring the father’s exposures. Nevertheless, causes of fetal loss are still most often investigated only in mothers. Paternal risk factors for fetal loss have been scarcely explored, particularly occupational exposures. Though, males appear to be more exposed to occupational reprotoxic agents than females and are not always aware or sufficiently informed of these exposures. Reprotoxic mechanisms of father’s occupational exposures may include sperm nucleus alteration, seminal fluid contamination and/or indirect exposure of the mother to paternal occupational environment (via linen, dust…). Study design, size, duration A systematic review of the literature using PRISMA 2020 methodology was performed for full text English and French language articles in the Pubmed MEDLINE, Google Scholar, Web of Science and Embase databases. Participants/materials, setting, methods We included only original studies published until December 2022, performed in humans, including a control group and performing a multivariate analysis. The fetal losses analysed were early and/or late and we did not exclude studies analysing stillbirths. We excluded studies in which the female partner was also occupationally exposed. The dose-response relationship and mechanisms of action were noted where described. Main results and the role of chance The 33 studies included analysed a total of 540,246 pregnancies from 8,183 couples or 114,093 exposed male workers, and were classified into 3 groups according to the occupational hazards studied. Regarding chemical agents, the risk of miscarriage was significantly increased in cases of paternal occupational exposure to Thiocarbamate(OR = 1.9, 95% CI 1.1-3.3), Carbaryl (OR = 1.9, 95% CI 1.9-3.1), Dichloro-Diphenyl-Trichloroethane (OR = 1.57, 95% CI 1.13-2.18), printing solvents (OR = 5.5, 95% CI 1.8-17.2), ethylene oxide (OR = 4.7, 95% CI 1.2-18.4), petroleum refinery solvents (OR = 2.2, 95% CI 1.3-3.8) and stainless steel welding fumes (RR = 3.5, 95% CI 1.3-9.1). Regarding physical agents, the risk of stillbirth or perinatal mortality was significantly increased with exposure to ionising (OR = 1.86, 95% CI 1.21-2.76) and nonionising radiation (RR = 2.23, 95% CI 1.08-4.62). Regarding the type of occupation, the risk of miscarriage or stillbirth was significantly increased among crushers, grinders and calenders (OR = 2.20, 95% CI 1.13-4.30), to seamstresses (OR = 2.54, 95% CI 1.29-5), sheet metal workers and commercial aircrew (OR = 2.85, 95% CI 1.30-6.23). The dose-response relationships showed divergent results. The mechanisms of action hypothesized were mainly germ cell mutations. Limitations, reasons for caution The publications selected were mostly published before 2010 and showed high variation in the population sizes, types of male occupational exposure, and in the nature and number of confounding factors used for the multivariate statistical analysis. Due to the various nature of exposures analysed, no meta-analysis could be performed. Wider implications of the findings Men should be made more aware of male-mediated occupational reproductive risks. Occupational health professionals should participate in the investigation of the causes of foetal loss and act on male occupational exposures that may impact pregnancy outcomes. Further high-powered prospective studies are needed, which should include paternal current occupational exposures. Trial registration number not applicable

Parental occupational exposure to metals and risk of cancer in the offspring: A register-based case-control study from Sweden

BackgroundCancer risks in the offspring of mothers and fathers exposed to metals are unknown. We estimated the relative risks of childhood cancer, overall and by type, associated with parental occupational exposure to arsenic, cadmium, chromium, nickel, and lead. MethodsWe conducted a nested case-control study (1960–2015) of children born in Sweden aged 0–19 years diagnosed with cancer (National Cancer Register) matched 25:1 to controls on birth year and sex. We obtained parental occupational data around their birth from censuses and a nationwide register and identified exposure to each metal (yes/no, or higher/lower/no exposure) using the Swedish job-exposure matrix (SWEJEM). Adjusted odds ratios (OR) and 95% confidence intervals (CIs) were estimated separately for maternal and paternal exposures using conditional logistic regression. ResultsWe compared 9653 cases to 1,72,194 controls in maternal and 12,521 cases to 2,74,434 controls in paternal analyses, respectively. We found a 38% increased risk of cancer associated with maternal occupational exposure to arsenic (OR 1.38 [95% CI 1.06, 1.82]), likely driven by higher risks for lymphoma (OR 1.52 [0.73, 3.15]), central nervous system (CNS) (OR 1.49 [0.88, 2.54]) and other solid malignancies (OR 1.74 [1.14, 2.65]). There were also indications of higher risks of lymphoma in children of mothers exposed to nickel and iron, and of CNS tumours due to chromium exposure. No associations were observed from paternal occupational exposure to any of the metals. ConclusionsWe found evidence of increased risks of cancer in children of mothers but not fathers occupationally exposed to arsenic and potentially other metals.

Paternal occupational exposures and infant congenital heart defects in the Japan Environment and Children’s Study

Few prospective studies have investigated the association between paternal occupational exposures and risk of infant congenital heart defects (CHDs). We investigated the associations between paternal occupational exposures, frequency of use, and concurrent or sequential exposure to a mixture of compounds and the risk of infant CHDs. Our study examined 28,866 participants in the Japan Environment and Children's Study. Logistic regression analysis was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) associated with paternal occupational exposures during the 3 months until pregnancy was noticed after adjustment for potential confounding factors of the infant CHDs. CHD diagnosis was ascertained from medical record. In total, 175 were diagnosed with infant CHDs. The number of fathers who were exposed to the following substances at least once a month were: 11,533 for photo copying machine/laser printer, 10,326 for permanent marker, 8,226 for soluble paint/inkjet printer, 6,188 for kerosene/petroleum/benzene/gasoline, 4,173 for organic solvents, 3,433 for chlorine bleach/germicide, 2,962 for engine oil, 2,931 for insecticide, 2,460 for medical sterilizing disinfectant, 1,786 for welding fumes, 1,614 for dyestuffs, 1,247 for any products containing lead-like solder, 986 for herbicide, 919 for radiation/radioactive substances/isotopes, 837 for lead-free solder, 341 for microbes, 319 for formalin/formaldehyde, 301 for agricultural chemical not listed above or unidentified, 196 for general anesthetic for surgery at hospital, 171 for anti-cancer drug, 147 for chromium/arsenic/cadmium, 88 for mercury and 833 for other chemical substances. Paternal occupational exposure regularly to photo copying machine or laser printer and soluble paint/inkjet printer were associated with higher risks of infant CHDs: the adjusted ORs (95%CIs) were 1.38 (1.00-1.91) and 1.60 (1.08-2.37), respectively. The higher risks were also observed for occasional exposure to engine oil, any products containing lead-like solder lead-free solder, and microbes; the adjusted ORs (95%CIs) were 1.68 (1.02-2.77), 2.03 (1.06-3.88), 3.45 (1.85-6.43), and 4.51, (1.63-12.49), respectively. Periconceptional paternal occupational exposure was associated with a higher risk of infant CHDs. Further studies using biomarkers of the association between paternal occupational exposure and infant CHDs are warranted.

Paternal Occupational Exposure to Heavy Metals and Welding Fumes and Testicular Germ Cell Tumours in Sons in France.

Simple SummaryTesticular cancer is the most common cancer among men below 40 years old, and its causes remain largely unknown. Marked geographic differences in the occurrence along with the relatively young age at diagnosis suggest a possible role of environmental and occupational exposures that occur early in life, probably already during embryonic development. Using data from a French case–control study, we investigated associations between paternal occupational exposure to five heavy metals and welding fumes before and at birth and testicular cancer risk in sons. We estimated exposures from job titles and considered other potential risk factors in the statistical analyses. We found no association. Thus, further research is necessary to identify potentially modifiable risk factors.Testicular cancer is the most common cancer in young men. Its causes are largely unknown, although prenatal occupational and environmental exposures have been suggested. We investigated paternal occupational exposure to heavy metals and welding fumes and the risk of testicular germ cell tumors (TGCT) in their offspring. A total of 454 cases and 670 controls were included from a French nationwide case–control study. The INTEROCC job exposure matrix was used to assign occupational exposures (cadmium, chromium, iron, nickel, lead, and welding fumes) to the fathers’ jobs. Odds ratios (ORs) for TGCT were estimated using conditional logistic regression models for frequency-matched sets. Three complementary analytical approaches were used: (1) single-agent analysis, (2) analysis by groups, and (3) principal component analysis (PCA). The proportion of paternal exposure to different heavy metals and welding fumes ranged from 0.7% (cadmium) to 11.3% (lead). Based on PCA, three principal components explained 93.5% of the cumulative variance. No associations were found between heavy metals or welding fumes and TGCT. In this study, paternal occupational exposure to heavy metals or welding fumes was not associated with TGCT development in their sons.

Parental occupational exposure to combustion products, metals, silica and asbestos and risk of childhood leukaemia: Findings from the Childhood Cancer and Leukaemia International Consortium (CLIC).

Parental occupational exposures around conception (father) or during pregnancy (mother) have been hypothesized as potential predisposing factors for childhood leukaemia. We investigated parental exposure to several known occupational carcinogens and childhood leukaemia risk. We conducted a pooled analysis using case-control data from four European countries (3362 childhood leukemia cases and 6268 controls). Parental occupational exposures to polycyclic aromatic hydrocarbons (PAH), diesel engine exhaust (DEE), chromium, nickel, crystalline silica, and asbestos were assessed by a general population job-exposure matrix. We estimated odd ratios (ORs) and 95% confidence intervals (CIs) using unconditional logistic regression models for all childhood leukaemia combined, by leukaemia type (ALL and AML) and by ALL subtype (B-lineage and T-lineage). We found an association between high paternal occupational exposure to crystalline silica and childhood ALL (OR 2.20, CI 1.60–3.01) with increasing trend from no exposure to high exposure (P = <0.001), and also for AML (OR 2.03, CI 1.04–3.97; P for trend = 0.008). ORs were similar for B- and T-lineage ALL. For ALL, ORs were also slightly elevated with wide confidence intervals for high paternal occupational exposure to chromium (OR 1.23, CI 0.77–1.96), and DEE (OR 1.21, CI 0.82–1.77). No associations were observed for paternal exposures to nickel, PAH and asbestos. For maternal occupational exposure we found several slightly elevated odds ratios but mostly with very wide confidence intervals due to low numbers of exposed mothers. This is a first study suggesting an association between fathers’ occupational exposure to crystalline silica and an increased risk of childhood leukaemia in their offspring. As this association was driven by certain occupations (field crop farmers and miners) where other potentially relevant exposures like pesticides and radon may also occur, more research is needed to confirm our findings of an association with crystalline silica, and if so, mechanistic studies to understand the pathways.

Occupational exposure to pesticides in mothers and fathers and risk of cancer in the offspring: A register-based case-control study from Sweden (1960–2015)

Maternal and paternal occupational exposure to pesticides was linked to leukemia in the offspring in some previous studies. Risks for other cancers, particularly from maternal exposure, are largely unknown. We examined the association between maternal and paternal exposure to pesticides and childhood cancer in a Swedish register-based case-control study (1960–2015). Cancer cases <20 years old were identified from the Cancer Register (n = 17313) and matched to controls (1:25) on birth year and sex. Employment history of each biological parent around the child's birth was retrieved from six censuses and a nationwide register, and exposure to any of herbicides, insecticides, and fungicides was evaluated using the Swedish job-exposure matrix (SWEJEM) in 9653/172194 mothers and 12521/274434 fathers of cases/controls. Adjusted odds ratios (OR) and 95% confidence intervals (CI) were estimated from conditional logistic regression models for any cancer, leukemia, lymphoma, central nervous system [CNS], and other solid tumors. We found an OR of 1.42 (95% CI 0.78, 2.57; 12 exposed cases) for lymphoma and 1.30 (95% CI 0.88, 1.93; 27 exposed cases) for other solid tumors associated with maternal occupational exposure to pesticides. No associations were observed between maternal exposure and leukemia or CNS tumors, or paternal exposure and any of the cancers examined, except for a potential association between pesticides exposure and myeloid leukemia (OR 1.15 [95% CI 0.73, 1.79; 22 exposed cases]). Although these findings merit further investigation, they indicate that parental exposure to pesticides may lead to higher risks of childhood cancer even in settings of low exposure.

Urinary Pb levels in schoolchildren from the largest coal mining area in Brazil and its associated factors: a cross-sectional study.

Candiota region has the largest coal reserve in Brazil, and previous studies have shown moderate-high levels of metals in the environment, including Pb. On the other hand, there are no studies investigating the factors associated with high levels of urinary Pb in children in the region. To investigate this issue, a cross-sectional study was conducted with 92 schoolchildren from 7 cities comprising this coal-mining region. Socioeconomic and demographic information and parental life habits and children's health information were collected using a semi-structured questionnaire. Diurnal urine samples were collected to quantify Pb levels (µg/g creatinine). Bi- and multivariate Poisson regression with a robust estimator was used to assess factors associated with high levels of Pb. Urinary Pb levels in children in the region vary from not detected to 21.6µg/g of creatinine. The spatial distribution of urinary Pb levels in children indicated an influence of proximity to mining areas, and this factor was confirmed by Poisson regression analysis (bivariate). Other factors associated with high levels of urinary Pb were non-white mothers, paternal occupational exposure, and low BMI. The findings of this study reveal that the Candiota region is a hotspot for high levels of urinary Pb in children (geometric mean: 3.82µg/g creatinine) and that, in addition to the proximity to mining areas, factors socioeconomic and health conditions may be associated with these high levels.

Predicting the Risk of Microtia From Prenatal Factors: A Hospital-Based Case-Control Study

BackgroundAlthough a wide range of risk factors for microtia were identified, the limitation of these studies, however, is that risk factors were not estimated in comparison with one another or from different domains. Our study aimed to uncover which factors should be prioritized for the prevention and intervention of non-syndromic microtia via tranditonal and meachine-learning statistical methods.Methods293 pairs of 1:1 matched non-syndromic microtia cases and controls who visited Shanghai Ninth People's Hospital were enrolled in the current study during 2017-2019. Thirty-nine risk factors across four domains were measured (i.e., parental sociodemographic characteristics, maternal pregnancy history, parental health conditions and lifestyles, and parental environmental and occupational exposures). Lasso regression model and multivariate conditional logistic regression model were performed to identify the leading predictors of microtia across the four domains. The area under the curve (AUC) was used to calculate the predictive probabilities.ResultsEight predictors were identified by the lasso regression, including abnormal pregnancy history, genital system infection, teratogenic drugs usage, folic acid supplementation, paternal chronic conditions history, parental exposure to indoor decoration, paternal occupational exposure to noise and maternal acute respiratory infection. The additional predictors identified by the multivariate conditional logistic regression model were maternal age and maternal occupational exposure to heavy metal. Predictors selected from the conditional logistic regression and lasso regression both yielded AUCs (95% CIs) of 0.83 (0.79–0.86).ConclusionThe findings from this study suggest some factors across multiple domains are key drivers of non-syndromic microtia regardless of the applied statistical methods. These factors could be used to generate hypotheses for further observational and clinical studies on microtia and guide the prevention and intervention strategies for microtia.

Potential occupational exposure of parents to endocrine disrupting chemicals, adverse birth outcomes, and the modification effects of multi-vitamins supplement and infant sex

BackgroundMaternal occupational exposure to endocrine disrupting chemicals (EDCs) may have adverse effect on birth outcomes. However, little is known about paternal EDCs exposure and the combined effect of parental exposure on birth outcomes. ObjectivesTo assess the effects of both maternal and paternal occupational EDCs exposure on adverse birth outcomes, and further explore if multi-vitamins supplement and infant sex modify the association. MethodsWe conducted a prospective cohort study of 5421 mother-father-newborn groups in Guangzhou, China. A questionnaire informed by a job exposure matrix (JEM) was applied to collect parental occupational EDCs exposure based on the type of work performed. We used logistic regression to estimate association between parental EDCs exposure and birth outcomes (including preterm birth (PTB), low birth weight (LBW), birth defects and congenital heart defects (CHD)). Stratified analyses and Cochran Q tests were performed to assess the modifying effect of maternal multi-vitamins supplement use and infant sex. ResultsCompared with mothers unexposed, we found that mothers those exposed to EDCs were associated with increased odds of birth defects (aOR=1.70, 95% confidence interval (CI): 1.10–2.62), especially for those exposed for > 1.5 years (aOR= 3.00, 95% CIs: 1.78–5.03), or those with directly occupational exposed to EDCs (aOR= 2.94, 95% CIs: 1.72–5.04). Maternal exposure for > 1.5 years and direct exposure increased the risk of CHD, with aORs of 2.47 (1.21–5.02) and 2.79 (1.37–5.69), respectively. Stronger adverse effects were also observed when mothers and fathers were both exposed to EDCs. Paternal occupational EDCs exposure and exposure ≤ 1.5 years was associated with increased odds of LBW, with aORs of 2.14 (1.63–2.79) and 1.54 (1.10–2.15), respectively. When stratified by multi-vitamins supplement and infant sex, we observed slightly stronger effects for maternal exposure on birth defects/CHD as well as paternal EDCs exposure on PTB and LBW, among those without multi-vitamins supplement and among male babies, although the modification effects were not significant. ConclusionMaternal exposure to EDCs was associated with greater odds of birth defects and CHD, while paternal exposure was mainly associated with greater odds of LBW. These effects tend to be stronger among mothers without multi-vitamins supplement and among male babies.

Childhood cancer risk in offspring of parents occupationally exposed to dusts: A register-based nested case-control study from Sweden of 5 decades.

BackgroundSome largely inconsistent associations between parental occupational dust exposure and childhood cancer have been reported, with maternal exposures inadequately studied. The authors examined whether maternal or paternal occupational exposure to animal, wood, textile, or paper dust around a child's birth was associated with an increased risk of childhood cancer, both overall and by type (leukemias, lymphomas, central nervous system tumors, and other cancers).MethodsIn this nationwide, register‐based, case‐control study, children who were diagnosed with cancer from 1960 to 2015 were compared with up to 25 matched controls regarding maternal and paternal occupational dust exposure (9653 cases in maternal analyses and 12,521 cases in paternal analyses). Exposures were assessed using a job‐exposure matrix and occupational information from census and register data. By using conditional logistic regression models, adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated.ResultsNeither maternal nor paternal occupational exposure to animal, wood, textile, or paper dust was associated with childhood cancer overall, leukemias, or central nervous system tumors. Maternal, but not paternal, wood dust exposure was associated with an increased risk of lymphoma (OR, 1.42; 95% CI, 1.10‐1.84), particularly non‐Hodgkin lymphoma (OR, 2.03; 95% CI, 1.21‐3.40).ConclusionsThe current study did not confirm the associations reported previously but is the first to suggest a link between maternal occupational exposure to wood dust around pregnancy and lymphoma in the offspring.

Parental occupation and childhood germ cell tumors: a case\u2013control study in Denmark, 1968\u20132016

PurposeTo examine associations between parental occupation and childhood germ cell tumors (GCTs) in offspring while distinguishing by common histologic subtype (i.e., yolk sac tumor and teratoma).MethodsThis population-based case–control study included childhood GCT cases in Denmark diagnosed 1968–2015 (< 16 years old at diagnosis) and sex and birth year-matched controls. Demographic information and parental employment histories were obtained from Danish registries. Parental occupation was assessed by industry; job-exposure matrices were used to examine specific occupational exposures (i.e., potentially carcinogenic organic solvents and social contact). Conditional multivariable logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (CIs).ResultsOverall, 178 childhood GCT cases (50 yolk sac tumors; 65 teratomas) and 4,355 controls were included for analysis. Maternal employment in education during pregnancy was associated with offspring GCTs (OR 2.45, 95% CI 1.23–4.90), especially yolk sac tumors (OR 5.27, 95% CI 1.94–14.28). High levels of both maternal and paternal occupational social contact were also associated with offspring yolk sac tumors across all exposure periods (ORs 2.30–4.63). No signals were observed for paternal occupational solvent exposure, while imprecise associations were estimated for maternal exposure (e.g., dichloromethane exposure during pregnancy, OR 1.51, 95% CI 0.77–2.95).ConclusionOur findings suggest that parental occupation is associated with offspring GCTs, with most consistent evidence supporting an association between maternal employment in education or other high social contact jobs and offspring yolk sac tumors.

Follow-Up of Elevated Blood Lead Levels and Sources in a Cohort of Children in Benin.

Lead exposure is associated with poor cognitive development in children. Very few studies in sub-Saharan Africa (SSA) have studied blood lead levels (BLLs) and non-gasoline sources of exposure in children. Data from a birth cohort in Benin (2011–2013) suggested that 58% of 1-year-old children had BLLs > 50 ug/L. We aimed to investigate the prevalence of elevated BLLs (>50 µg/L and >100 µg /L) among 425 of these children at 6 years of age in 2016–2018 and to compare BLLs between age 1 and 6 years, and study sources of lead at age 6 years. BLLs were analysed by inductively coupled plasma mass spectrometry. Multiple linear regression and quantile regressions were used to study potential sources of lead. The prevalence of BLLs > 50 µg/L in children was 59.5% (Geometric Mean (GM) 56.4 µg/L, 95% CI: 54.1–58.7) at 6 years of age compared to 54.8% (GM 56.5 µg/L, 95% CI: 53.4–59.6) at 1 year of age. The prevalence of children with BLLs > 100 µg/L decreased from 14.4% at 1 year of age to 8.2% at 6 years of age. After adjustment for all other covariates, consumption of peanuts more than once per month was significantly associated with a 22.0% (95% CI: 4.6, 42.5) increment in BLLs at age 6 years compared with no consumption. Consumption of bushmeat killed by lead bullets at age 6 years was associated with an increase in the higher percentiles of BLLs (P75) compared with the absence of this source. Other potential sources of lead associated with BLLs with marginal significance were consumption of rice, paternal occupational exposure, and the presence of activity with the potential use of lead. This prospective cohort confirms the persistently high prevalence of elevated BLLs in children residing in a rural region in the south of Benin, as well as the presence of multiple and continuous sources of lead. These results highlight the need for prevention programs to reduce and eliminate lead exposure in children.

Metal mining and birth defects: a case-control study in Lubumbashi, Democratic Republic of the Congo

Widespread environmental contamination caused by mining of copper and cobalt has led to concerns about the possible association between birth defects and exposure to several toxic metals in southern Katanga, Democratic Republic of the Congo (DRC). We therefore aimed to assess the possible contribution of parental and antenatal exposure to trace metals to the occurrence of visible birth defects among neonates. We did a case-control study between March 1, 2013, and Feb 28, 2015, in Lubumbashi, DRC. We included newborns with visible birth defects (cases) and healthy neonates born in the same maternity ward (controls). Mothers were interviewed about potentially relevant exposures, including their partners' jobs. Various trace metals were measured by inductively coupled plasma mass spectrometry in maternal urine, maternal blood, umbilical cord blood, placental tissue, and surface dust at home. Multivariable logistic regression analyses were done to calculate adjusted odds ratios and their 95% CIs (CI). Our study included 138 neonates with visible birth defects (about 0·1% of the 133 662 births in Lubumbashi during the study period) and 108 control neonates. Potential confounders were similarly distributed between cases and controls. Vitamin consumption during pregnancy was associated with a lower risk of birth defects (adjusted odds ratio 0·2, 95% CI 0·1-0·5). Mothers having paid jobs outside the home (2·8, 1·2-6·9) and fathers having mining-related jobs (5·5, 1·2-25·0) were associated with a higher risk of birth defects. We found no associations for trace metal concentrations in biological samples, except for a doubling of manganese (Mn; 1·7, 1·1-2·7) and zinc (Zn; 1·6, 0·9-2·8) in cord blood. In a separate model including placentas, a doubling of Mn at the fetal side of the placenta was associated with an increased risk of birth defects (3·3, 1·2-8·0), as was a doubling of cord blood Zn (5·3, 1·6-16·6). To our knowledge, this is the first study of the effects of mining-related pollution on newborns in sub-Saharan Africa. Paternal occupational mining exposure was the factor most strongly associated with birth defects. Because neither Mn nor Zn are mined in Lubumbashi, the mechanism of the association between their increased prenatal concentrations and birth defects is unclear. Flemish Interuniversity Council-University Development Cooperation, The Coalition of the North-South movement in Flanders 11.11.11.

Case\u2013control study of paternal occupational exposures and childhood\xa0bone tumours and soft-tissue sarcomas in Great Britain, 1962\u20132010

BackgroundThis nationwide study investigated associations between paternal occupational exposure and childhood bone tumours and soft- tissue sarcomas.MethodsThe UK National Registry of Childhood Tumours provided cases of childhood sarcomas born and diagnosed in Great Britain, 1962–2010. Control births, unaffected by childhood cancer, were matched on sex, birth period and birth registration sub-district. Fathers’ occupations were assigned to one or more of 33 exposure groups and coded for occupational social class.ResultsWe analysed 5,369 childhood sarcoma cases and 5380 controls. Total bone tumours, total soft-tissue sarcomas and the subgroups osteosarcoma, rhabdomyosarcoma and Ewing Sarcoma Family of Tumours (ESFT) were considered separately. Significant positive associations were seen between rhabdomyosarcoma and paternal exposure to EMFs (odds ratio = 1.67, CI = 1.22–2.28) and also for ESFT and textile dust (1.93, 1.01–3.63). There were putative protective effects on total bone tumours of paternal dermal exposure to hydrocarbons, metal, metal working or oil mists.ConclusionsDespite the large size and freedom from bias of this study, our results should be interpreted with caution. Many significance tests were undertaken, and chance findings are to be expected. Nevertheless, our finding of associations between ESFT and paternal exposure to textile dust may support related suggestions in the literature.

Occupational livestock or animal dust exposure and offspring cancer risk in Denmark, 1968-2016.

To examine associations with occupational livestock or other animal dust exposure and offspring cancer risk. In this population-based case-control study of Danish children aged < 17years old, 5078 childhood cancer cases diagnosed 1968-2016 were matched to cancer-free controls by birth year and sex (n = 123,228). Occupational livestock or animal dust exposure was identified using a job-exposure matrix. We employed multivariable conditional logistic regression models to estimate associations with offspring cancer for births 1968-2016 and 1989-2016, with the latter timeframe reflecting a period of presumed higher exposure due to changes in Danish farming practices. Sensitivity analyses considered place of birth (urban areas vs. rural areas and small towns). For births 1968-2016, paternal exposure from offspring birth to cancer diagnosis was associated with central nervous system tumors (adjusted odds ratio [OR] = 1.30, 95% confidence interval [CI] 1.04-1.63) and germ cell tumors (OR = 1.82, 95% CI 1.05-3.27), while maternal pregnancy exposure was associated with astrocytoma (OR = 1.89, 95% CI 1.00-3.57). For births 1989-2016, paternal exposure from offspring birth to cancer diagnosis was negatively associated with acute lymphoid leukemia (OR = 0.58, 95% CI 0.33-1.00). For births in rural areas only, maternal exposure from offspring birth to cancer diagnosis was positively associated with acute myeloid leukemia (OR = 2.16, 95% CI 1.09-4.29). This study suggests that paternal occupational animal exposure is associated with offspring germ cell tumors, and maternal pregnancy exposure with astrocytomas. Our results are mixed with respect to leukemia subtypes.

Paternal occupational exposure to chemicals and secondary sex ratio: results from the Japan Environment and Children's Study

Declining proportions of male births have been reported in several industrialised countries. Previous reports have shown that exposure to certain chemical substances might influence the secondary sex ratio (SSR). We assessed the associations between paternal occupational exposure to chemicals and the SSR of their children using the Japan Environment and Children's Study (JECS), a large-scale birth cohort study. Data on paternal occupational exposure to various agents and other covariates were collected using a self-administered questionnaire to partners of pregnant female participants enrolled in the JECS. After adjusting for potential confounders, multivariable modified Poisson regression models were used to evaluate associations between paternal occupational exposures and the SSR of their children. This study was registered in the UMIN Clinical Trials Registry, number UMIN000030786. The JECS study gathered data on 103 062 pregnancies, 104 065 fetuses, and 51 898 partners of pregnant women. Among 50 283 children with data on paternal occupational exposures, 25 657 were male and 24 626 were female. The proportion of boys whose fathers were regularly occupationally exposed to insecticides was 0·445 (males, n=293; females, n=366; 95% CI 0·406-0·483), which was lower than the proportion of boys whose fathers were not exposed to insecticides. After adjusting for confounding factors, regular paternal occupational exposure to insecticides (adjusted relative risk 0·86, 95% CI 0·78-0·96) and medical disinfectants (0·95, 0·90-1·00) were significantly associated with lower SSRs among their offspring compared with the offspring of fathers not exposed to these substances. A declining proportion of boys could potentially be due to fathers working in environments in which they are exposed to chemicals. The associations between poorer semen quality and levels of reproductive and thyroid hormones require investigation. Ministry of the Environment of Japan.

A National Study of Maternal and Paternal Occupational Exposure to Endocrine Disrupting Chemicals and Pregnancy Outcomes

A National Study of Maternal and Paternal Occupational Exposure to Endocrine Disrupting Chemicals and Pregnancy Outcomes

Occupational exposure to endocrine-disrupting chemicals and other parental risk factors in hypospadias and cryptorchidism development: a case–control study

Endocrine-disrupting chemicals (EDCs) are exogenous agents that are capable of altering the endocrine system functions, including the regulation of developmental processes. The aim of this study was to investigate the association between EDCexposure and other parental factors in the etiology of hypospadias and cryptorchidism. A case-control study was conducted. Cases (n = 210) were infants aged between 6 months and 14 years diagnosed with hypospadias or cryptorchidism who attended the authors' hospital over a period of 18 months, and controls (n = 210) were infants within the same range of age and without any urological disorders who attended the outpatient clinic of the same hospital during the same time period. Their selection was independent of exposures. Data on parental occupational exposure to EDCs and other sociodemographic variables were collected through face-to-face interviews and systematically for both cases and controls. Crude and adjusted odds ratios (ORs) were estimated to control for confounding with their 95% confidence interval (CI) by means of logistic regressions. Specifically, three final models of a dichotomous outcome were constructed: one for cryptorchidism, one for hypospadias, and the third considering both malformations together. The Hosmer-Lemeshow test was used to assess the goodness of fit of the models. Their discriminatory accuracy (DA) was ascertained by estimating their areas under the receiver operating characteristiccurves area under the curve (AUC) along with their 95% CI. Associations were found between advanced maternal age (OR adjusted=1.82; 95% CI: 1.14-2.92), mother's consumption of anti-abortives (OR=5.40; 95% CI: 1.40-38.5) and other drugs (OR=2.02; 95% CI: 1.31-3.16) during pregnancy, maternal and paternal occupational exposure to EDCs (OR = 4.08; 95% CI: 2.03-8.96 and OR = 3.90; 95% CI: 2.41-6.48, respectively), fathers smoking (OR=2.0; 95% CI: 1.33-2.99), and fathers with urological disorders (OR=2.31; 95% CI: 1.15-4.90). Maternal and paternal high educational level could be protective of cryptorchidism (OR=0.47; 95% CI: 0.28-0.76and OR=0.63; 95% CI: 0.42-0.93, respectively). The DA of the models for the whole sample (AUC=0.75; 95% CI: 0.70-0.79)for cryptorchidism (AUC = 0.76; 95% CI: 0.71-0.82)and for hypospadias (AUC = 0.75; 95% CI: 0.69-0.81) was moderately high. Advanced age, some parental occupational exposure to EDCs, some drugconsumption, smoking, and the father's history of urological disorders may increase risk and predict the developments of these malformations. Studies with higher samples sizes are needed to assess associations between individual EDC occupational exposures and drugs and these malformations.