Relationship Between Environmental Air Quality and Congenital Heart Defects.

The condition was rare, so only 113 cases and 550 controls were analysed for PM 2.5, and only 68 cases and 352 controls for ozone in Weeks 3-8. The study grouped 13 different critical congenital heart defects together, so a link with one defect could be hidden. Controls were geocoded to census tract centroids rather than home addresses because residential addresses were not available from vital statistics. Exposure was estimated from outdoor monitors near the residence, not from time spent indoors, at work, in transit, or after moving. Air pollution levels were below EPA standards, so the study cannot address higher urban or industrial exposures. Ozone monitoring was unavailable from November through February, and infants with critical exposure windows then were excluded. Important risk factors such as maternal smoking, occupational exposures, diet, obesity, diabetes, socioeconomic status, and family history were not available. The design was retrospective and cannot show that air pollution caused congenital heart defects; the week-specific results were additional analyses, not the primary models.

The article text does not report a conflicts-of-interest declaration. The supplied metadata says the work had research support from the National Institutes of Health, Extramural.

Do not read the Week 5 and Week 8 PM 2.5 results as proof that air pollution causes critical congenital heart defects. The primary models covering Weeks 3-8 and Weeks 1-12 were not significant, and the study was retrospective with low pollution levels.