Placental diffusing capacities at varied carbon monoxide tensions.

Bissonnette, John M.; Wickham, Walter K.; Drummond, Willa H.

doi:10.1172/jci108726

Cited by 10 publications

(4 citation statements)

References 20 publications

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“…The relative affinity of CO for hemoglobin is 200-fold greater than that of oxygen (Rodkey et al, 1974), and it decreases the oxygen carrying capacity of the hemoglobin. Carbon monoxide easily crosses the placenta either by diffusion (Longo, 1977) or via a carrier (Bissonnette et al, 1977) and enters the fetal blood. Once in the fetal blood, the CO transfer from fetus to mother is decreased at increased CO tensions.…”

Section: Discussionmentioning

confidence: 99%

Gastroschisis is caused by the combination of carbon monoxide and protein‐zinc deficiencies in mice

Singh

2003

Birth Defects Research Pt B

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Section: Discussionmentioning

confidence: 99%

Gastroschisis is caused by the combination of carbon monoxide and protein‐zinc deficiencies in mice

Singh

2003

Birth Defects Research Pt B

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“…Gas transfer from the maternal circulation to the fetus is determined by uterine and umbilical blood flow, maternal and fetal capacity and affinity for the specific gas, oxygen consumption of the placenta, and placental diffusing capacity (Bissonnette, 1977b; Carter, 1999). Placental diffusing capacity is the quantity of gas that crosses the placenta over time and is influenced by surface area, thickness and solubility of the tissue membranes, diffusion properties of the gas, and distribution of fetal and maternal blood within the placental capillaries (Carter, 1999).…”

Section: Environmental Co and Overt Toxicitymentioning

confidence: 99%

“…Placental diffusing capacity is the quantity of gas that crosses the placenta over time and is influenced by surface area, thickness and solubility of the tissue membranes, diffusion properties of the gas, and distribution of fetal and maternal blood within the placental capillaries (Carter, 1999). Following maternal exposure to CO and formation of maternal COHb, CO readily diffuses across the placenta and binds to fetal hemoglobin (Bissonnette, 1977b; McGregor, 1998). There is also evidence that transplacental CO diffusion may be facilitated by a carrier mediated process (Bissonnette, 1977b).…”

Section: Environmental Co and Overt Toxicitymentioning

confidence: 99%

“…Following maternal exposure to CO and formation of maternal COHb, CO readily diffuses across the placenta and binds to fetal hemoglobin (Bissonnette, 1977b; McGregor, 1998). There is also evidence that transplacental CO diffusion may be facilitated by a carrier mediated process (Bissonnette, 1977b). Placental diffusing capacity for CO has been found to increase during gestation, paralleling growth of the fetus (Bissonnette, 1977a).…”

Section: Environmental Co and Overt Toxicitymentioning

confidence: 99%

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Carbon monoxide pollution and neurodevelopment: A public health concern

Levy¹

2015

Neurotoxicology and Teratology

119

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Although an association between air pollution and adverse systemic health effects has been known for years, the effect of pollutants on neurodevelopment has been underappreciated. Recent evidence suggests a possible link between air pollution and neurocognitive impairment and behavioral disorders in children, however, the exact nature of this relationship remains poorly understood. Infants and children are uniquely vulnerable due to the potential for exposure in both the fetal and postnatal environments during critical periods in development. Carbon monoxide (CO), a common component of indoor and outdoor air pollution, can cross the placenta to gain access to the fetal circulation and the developing brain. Thus, CO is of particular interest as a known neurotoxin and a potential public health threat. Here we review overt CO toxicity and the policies regulating CO exposure, detail the evidence suggesting a potential link between CO-associated ambient air pollution, tobacco smoke, and learning and behavioral abnormalities in children, describe the effects of subclinical CO exposure on the brain during development, and provide mechanistic insight into a potential connection between CO exposure and neurodevelopmental outcome. CO can disrupt a number of critical processes in the developing brain, providing a better understanding of how this specific neurotoxin may impair neurodevelopment. However, further investigation is needed to better define the effects of perinatal CO exposure on the immature brain. Current policies regarding CO standards were established based on evidence of cardiovascular risk in adults with pre-existing comorbidities. Thus, recent and emerging data highlighted in this review regarding CO exposure in the fetus and developing child may be important to consider when the standards and guidelines are evaluated and revised in the future.

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Respiratory Gas Exchange in the Placenta

Longo

1987

Comprehensive Physiology

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Placental diffusing capacities at varied carbon monoxide tensions.

Cited by 10 publications

References 20 publications

Gastroschisis is caused by the combination of carbon monoxide and protein‐zinc deficiencies in mice

Gastroschisis is caused by the combination of carbon monoxide and protein‐zinc deficiencies in mice

Carbon monoxide pollution and neurodevelopment: A public health concern

Respiratory Gas Exchange in the Placenta

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