Increased risks of infant mortality and of deaths due to congenital malformation in the offspring of male electronics workers

Sung, Tzu I.; Wang, Jung‐Der; Chen, Pau‐Chung

doi:10.1002/bdra.20496

Cited by 25 publications

(17 citation statements)

References 36 publications

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“…We used standard international classifications both for the types of congenital malformations (ICD-10) and for parental occupations (ISCO-08). We assessed paternal workplace exposure during the periconceptional period as, depending on biological consideration and experimental evidence, most studies concentrated on the exposure period of 3 or 6 months before conception and the first trimester of pregnancy [17][18][19].…”

Section: Discussionmentioning

confidence: 99%

Paternal occupational exposures and the risk of congenital malformations — A case-control study

El-Helaly¹,

Abdel-Elah²,

Haussein³

et al. 2011

International Journal of Occupational Medicine and Environmental Health

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Objectives: This study examined the association between certain paternal occupational exposures during the periconceptional period and the risk of congenital malformations. Materials and Methods: A case-control study was carried out from December 2009 to April 2010; on 242 congenital malformation cases and 270 controls. Paternal occupational exposure to certain workplace hazards was assessed by a detailed questionnaire to evaluate the occupational exposure for both fathers and mothers including pesticides, solvents, welding fumes, lead, working with video display terminals (VDTs) and computer monitors. In addition, the questionnaire assessed the presence of other risk factors such as consanguinity, smoking and history of any maternal diseases during the pregnancy with the child. Results: The results revealed that the odds of having a child with congenital malformation was higher (P < 0.01) if the father was occupationally exposed to pesticides (OR: 3.42, 95% CI: 1.97-5.92), solvents (OR: 5.63, 95% CI: 2.77-11.42), or welding fumes (OR: 2.98, 0.99-8.54) during the periconceptional period. However, consanguinity (OR: 1.91, 95% CI: 1.25-2.92) was a risk factor of developing congenital malformations among offspring. Conclusion: Control of workplace exposures and adherence to threshold limit values of those hazards should be adopted to minimize the risk of developing congenital malformations among offspring.

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Section: Discussionmentioning

confidence: 99%

Paternal occupational exposures and the risk of congenital malformations — A case-control study

El-Helaly¹,

Abdel-Elah²,

Haussein³

et al. 2011

International Journal of Occupational Medicine and Environmental Health

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“…The evidence for this subfertility is shown by reduced sperm counts, sperm motility, and sperm morphology, increased anti-sperm antibodies, increased sperm reactive oxygen species, and DNA damage (6), which bare striking similarities to the subfertility phenotypes seen in obese men (52). Additionally, some paternal proinflammatory conditions, including smoking and environmental toxin exposure, are also associated with fathering children with increased susceptibility to cancer and childhood malformations (11,67). However, whether offspring health pathologies are programmed directly as a result of the proinflammatory state or another paternal phenotype that results from these conditions remains to be determined.…”

Section: Short-term Founder Diet/exercise Intervention Restored Adipomentioning

confidence: 99%

Preconception diet or exercise intervention in obese fathers normalizes sperm microRNA profile and metabolic syndrome in female offspring

McPherson

Owens

Fullston

et al. 2015

American Journal of Physiology-Endocrinology and Metabolism

169

150

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McPherson NO, Owens JA, Fullston T, Lane M. Preconception diet or exercise intervention in obese fathers normalizes sperm microRNA profile and metabolic syndrome in female offspring. Am J Physiol Endocrinol Metab 308: E805-E821, 2015. First published February 17, 2015 doi:10.1152/ajpendo.00013.2015.-Obesity and type 2 diabetes are increasingly prevalent across all demographics. Paternal obesity in humans and rodents can program obesity and impair insulin sensitivity in female offspring. It remains to be determined whether these perturbed offspring phenotypes can be improved through targeted lifestyle interventions in the obese father. Using a mouse model, we demonstrate that diet or exercise interventions for 8 wk (2 rounds of spermatogenesis) in obese founder males restores insulin sensitivity and normalized adiposity in female offspring. Founder diet and/or exercise also normalizes abundance of X-linked sperm microRNAs that target genes regulating cell cycle and apoptosis, pathways central to oocyte and early embryogenesis. Additionally, obesity-associated comorbidities, including inflammation, glucose intolerance, stress, and hypercholesterolemia, were good predictors for sperm microRNA abundance and offspring phenotypes. Interventions aimed at improving paternal metabolic health during specific windows prior to conception can partially normalize aberrant epigenetic signals in sperm and improve the metabolic health of female offspring. fertility; infertility; paternal programming; interventions; obesity THE INCIDENCE OF OBESITY HAS MORE THAN DOUBLED in children and tripled in adolescence (44). Obesity increases the risk of type 2 diabetes mellitus (T2DM), cancer, stroke, heart disease, and osteoarthritis in adulthood (49). It is widely accepted that increased maternal BMI and hyperglycemia during gestation or lactation is associated with obesity and T2DM in children through developmental programming separate from shared genetics or postnatal environment (27,48). Recent studies now suggest that paternal metabolic health at conception can also impact children's health, with obese fathers more likely to father an obese child (35). In rodents, diet-induced male obesity with or without diabetes induces a worsened metabolic phenotype in their female offspring, with glucose intolerance in female offspring due to pancreatic islet dysfunction and white adipose tissue dysfunction or insulin resistance and obesity, with some consequences evident across two generations (18,45,46). However, whether short-term lifestyle interventions in the obese father could rescue these programmed metabolic phenotypes in female offspring is currently unknown. This is an important question, because in western societies, greater than 70% of reproductive-aged men are overweight or obese (e.g., 74% in the US) (15, 44). Weight loss via diet and exercise interventions in obese men improves glucose control and insulin action (9), alters epigenetic marks (i.e., DNA methylation and microRNA) in their leucocytes (41,50), and also improves their r...

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“…There is also a known causal association between paternal age and significant medical conditions in the offspring such as autism (6). Similarly, children born to fathers of specific occupations have been shown to be at an increased risk for development of congenital abnormalities (7,8). Furthermore, there is also an association of increased paternal body mass index (BMI) around the time of conception with an increase in the BMI of the offspring (9,10).…”

mentioning

confidence: 95%

Paternal body mass index is associated with decreased blastocyst development and reduced live birth rates following assisted reproductive technology

Bakos

Henshaw

Mitchell

et al. 2011

Fertility and Sterility

202

172

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Increased risks of infant mortality and of deaths due to congenital malformation in the offspring of male electronics workers

Cited by 25 publications

References 36 publications

Paternal occupational exposures and the risk of congenital malformations — A case-control study

Paternal occupational exposures and the risk of congenital malformations — A case-control study

Preconception diet or exercise intervention in obese fathers normalizes sperm microRNA profile and metabolic syndrome in female offspring

Paternal body mass index is associated with decreased blastocyst development and reduced live birth rates following assisted reproductive technology

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