Spontaneous Abortion, Sex Ratio, and Paternal Occupational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin

Schnorr, Teresa M.; Lawson, Christina C.; Whelan, Elizabeth A.; Dankovic, David A.; Deddens, James A.; Piacitelli, Laurie A.; Reefhuis, Jennita; Sweeney, Marie Haring; Connally, L. Barbara; Fingerhut, Marilyn A.

doi:10.2307/3454859

Cited by 11 publications

(16 citation statements)

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“…In a study on sex ratio in children of men who worked in two plants producing Agent Orange, serum TCDD concentration at conception was calculated based on a pharmacokinetic model and TCDD levels in blood samples from 1987 (Schnorr et al., ). Men with no self‐reported occupational TCDD exposure served as matched reference population based on residence, age and race.…”

Section: Assessmentmentioning

confidence: 99%

Risk for animal and human health related to the presence of dioxins and dioxin‐like PCBs in feed and food

Knutsen¹,

Alexander²,

Barregård³

et al. 2018

EFS2

137

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The European Commission asked EFSA for a scientific opinion on the risks for animal and human health related to the presence of dioxins (PCDD/Fs) and DL‐PCBs in feed and food. The data from experimental animal and epidemiological studies were reviewed and it was decided to base the human risk assessment on effects observed in humans and to use animal data as supportive evidence. The critical effect was on semen quality, following pre‐ and postnatal exposure. The critical study showed a NOAEL of 7.0 pg WHO2005‐TEQ/g fat in blood sampled at age 9 years based on PCDD/F‐TEQs. No association was observed when including DL‐PCB‐TEQs. Using toxicokinetic modelling and taking into account the exposure from breastfeeding and a twofold higher intake during childhood, it was estimated that daily exposure in adolescents and adults should be below 0.25 pg TEQ/kg bw/day. The CONTAM Panel established a TWI of 2 pg TEQ/kg bw/week. With occurrence and consumption data from European countries, the mean and P95 intake of total TEQ by Adolescents, Adults, Elderly and Very Elderly varied between, respectively, 2.1 to 10.5, and 5.3 to 30.4 pg TEQ/kg bw/week, implying a considerable exceedance of the TWI. Toddlers and Other Children showed a higher exposure than older age groups, but this was accounted for when deriving the TWI. Exposure to PCDD/F‐TEQ only was on average 2.4‐ and 2.7‐fold lower for mean and P95 exposure than for total TEQ. PCDD/Fs and DL‐PCBs are transferred to milk and eggs, and accumulate in fatty tissues and liver. Transfer rates and bioconcentration factors were identified for various species. The CONTAM Panel was not able to identify reference values in most farm and companion animals with the exception of NOAELs for mink, chicken and some fish species. The estimated exposure from feed for these species does not imply a risk.

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Section: Assessmentmentioning

confidence: 99%

Risk for animal and human health related to the presence of dioxins and dioxin‐like PCBs in feed and food

Knutsen¹,

Alexander²,

Barregård³

et al. 2018

EFS2

137

View full text Add to dashboard Cite

show abstract

“…American veterans exposed to Agent Orange during defoliant sprayings in Vietnam (Operation Ranch Hand) with a level of exposure to TCDD of the same order of magnitude as in Seveso, Italy, had slightly more boys than girls [34]. Two recent studies of pesticide producers (2,4,5‐trichlorophenoxy acetic acid or trichlorophenol) in the USA [35] or in Russia [36] with much higher exposure levels showed discordant findings. Other persistent organochlorine compounds such as polychlorobiphenyls (PCB) have also been studied in particular in the populations highly exposed to contaminated rice oil in Yusho and Yucheng.…”

Section: Paternal Preconceptional Exposure: Human Evidencementioning

confidence: 99%

Evidence for a Role of Paternal Exposures in Developmental Toxicity

Cordier

2008

Basic Clin Pharma Tox

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Experimental evidence from radiation exposure, antimitotic drugs or chemicals such as pesticides or metals does suggest the possibility of transmission of paternally mediated developmental effects across generations. The mechanistic framework is growing with suggestion of transmission of epigenetic modifications as a mechanism alternative to germ-line mutagenesis. There is also ample experimental evidence for a specific susceptibility of the male embryo to the action of endocrine disrupters. In parallel, interpretation of epidemiological findings regarding effects of well-characterized paternal exposures, such as ionizing radiation or persistent organic pollutants (dioxins), on intrauterine development remains equivocal. Many epidemiological studies have included paternal exposures as an add-on to existing studies and focused mainly on birth defects, sex ratio, childhood cancers or spontaneous abortions. Functional alterations such as neurobehavioural parameters or reproductive dysfunction resulting from paternal exposure have been barely studied. Improved knowledge on possible consequences of paternal exposures in future generations is needed and has strong implication in terms of regulation, in the workplace for instance. One may expect human studies to be conducted with a particular focus on male-mediated developmental toxicity making use of biological markers pertinent to hypothesized mechanisms. Recognition of early determinants of disease onset has led to the setup of a number of mother-child cohorts across the world and careful assessment of paternal exposures should be included in these studies. These cohorts will also have the power to evaluate the specific impact of in utero exposure on a number of endpoints of developmental toxicity in males.

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“…In contrast to these studies, Karmaus et al 118) reported that paternal PCB exposure was linked to a higher population of male offsprings. Schnorr et al 119) studied the wives of 2,3,7,8tetrachloro-dibenzo-p-dioxin (TCDD) exposed chemical workers and wives of non-exposed neighborhood referents. No association between the paternal TCDD level at the time of conception and spontaneous abortion was observed among pregnancies fathered by workers with TCDD levels of <20 to 1,120 ppt compared to pregnancies fathered by referents.…”

Section: Other Occupational Situations Responsible For Reproductive Dmentioning

confidence: 99%

Occupational Exposure Associated with Reproductive Dysfunction

Kumar

2004

Journal of Occupational Health

168

114

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Spontaneous Abortion, Sex Ratio, and Paternal Occupational Exposure to 2,3,7,8-Tetrachlorodibenzo-p-Dioxin

Cited by 11 publications

References 0 publications

Risk for animal and human health related to the presence of dioxins and dioxin‐like PCBs in feed and food

Risk for animal and human health related to the presence of dioxins and dioxin‐like PCBs in feed and food

Evidence for a Role of Paternal Exposures in Developmental Toxicity

Occupational Exposure Associated with Reproductive Dysfunction

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