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Prenatal exposure to combustion-related air pollution may cause chromosomal abnormalities in fetal tissue, according to findings from a study of 60 New York City newborns.
In studies of other populations, such abnormalities have been linked to an increased risk of leukemia and other cancers, said Kirsti A. Bocskay of the department of environmental health sciences at Columbia University, New York, and her colleagues.
The investigators monitored exposure to polycyclic aromatic hydrocarbons (PAHs)—pollutants found in emissions from cars and other vehicles, residential heating, power generation, and tobacco smoking—among nonsmoking African American and Dominican mothers living in three low-income neighborhoods in the city.
The mothers filled out questionnaires and wore portable air monitors for 48 hours during the third trimester. Chromosomal abnormalities were measured in umbilical cord blood obtained at delivery.
The investigators found 4.7 chromosome abnormalities per 1,000 white blood cells in newborns from mothers with low exposure to PAHs and 7.2 abnormalities per 1,000 white blood cells in newborns from mothers with high exposure to PAHs.
(“Low” exposure meant air pollution levels below the average, while “high” exposure referred to above-average levels).
In particular, it was stable chromosomal aberrations—not unstable aberrations—that were increased. Stable aberrations are persistent, rather than transient, markers of cytogenetic damage.
“This study has demonstrated a significant association between prenatal environmental exposure to airborne carcinogenic PAHs and stable aberrations in cord blood at the relatively low environmental concentrations found in New York City,” the investigators said (Cancer Epidemiol. Biomarkers Prev. 2005;14:506–11).
Prenatal exposure to combustion-related air pollution may cause chromosomal abnormalities in fetal tissue, according to findings from a study of 60 New York City newborns.
In studies of other populations, such abnormalities have been linked to an increased risk of leukemia and other cancers, said Kirsti A. Bocskay of the department of environmental health sciences at Columbia University, New York, and her colleagues.
The investigators monitored exposure to polycyclic aromatic hydrocarbons (PAHs)—pollutants found in emissions from cars and other vehicles, residential heating, power generation, and tobacco smoking—among nonsmoking African American and Dominican mothers living in three low-income neighborhoods in the city.
The mothers filled out questionnaires and wore portable air monitors for 48 hours during the third trimester. Chromosomal abnormalities were measured in umbilical cord blood obtained at delivery.
The investigators found 4.7 chromosome abnormalities per 1,000 white blood cells in newborns from mothers with low exposure to PAHs and 7.2 abnormalities per 1,000 white blood cells in newborns from mothers with high exposure to PAHs.
(“Low” exposure meant air pollution levels below the average, while “high” exposure referred to above-average levels).
In particular, it was stable chromosomal aberrations—not unstable aberrations—that were increased. Stable aberrations are persistent, rather than transient, markers of cytogenetic damage.
“This study has demonstrated a significant association between prenatal environmental exposure to airborne carcinogenic PAHs and stable aberrations in cord blood at the relatively low environmental concentrations found in New York City,” the investigators said (Cancer Epidemiol. Biomarkers Prev. 2005;14:506–11).
Prenatal exposure to combustion-related air pollution may cause chromosomal abnormalities in fetal tissue, according to findings from a study of 60 New York City newborns.
In studies of other populations, such abnormalities have been linked to an increased risk of leukemia and other cancers, said Kirsti A. Bocskay of the department of environmental health sciences at Columbia University, New York, and her colleagues.
The investigators monitored exposure to polycyclic aromatic hydrocarbons (PAHs)—pollutants found in emissions from cars and other vehicles, residential heating, power generation, and tobacco smoking—among nonsmoking African American and Dominican mothers living in three low-income neighborhoods in the city.
The mothers filled out questionnaires and wore portable air monitors for 48 hours during the third trimester. Chromosomal abnormalities were measured in umbilical cord blood obtained at delivery.
The investigators found 4.7 chromosome abnormalities per 1,000 white blood cells in newborns from mothers with low exposure to PAHs and 7.2 abnormalities per 1,000 white blood cells in newborns from mothers with high exposure to PAHs.
(“Low” exposure meant air pollution levels below the average, while “high” exposure referred to above-average levels).
In particular, it was stable chromosomal aberrations—not unstable aberrations—that were increased. Stable aberrations are persistent, rather than transient, markers of cytogenetic damage.
“This study has demonstrated a significant association between prenatal environmental exposure to airborne carcinogenic PAHs and stable aberrations in cord blood at the relatively low environmental concentrations found in New York City,” the investigators said (Cancer Epidemiol. Biomarkers Prev. 2005;14:506–11).