Background Fast food consumption is associated with biomarkers of ortho-phthalates exposures. However, the chemical content of fast food is unknown; certain ortho-phthalates (i.e., di-n-butyl phthalate (DnBP) and di(2-ethylhexyl) phthalate (DEHP)) have been phased out and replaced with other plasticizers (e.g., dioctyl terephthalate (DEHT)). Objective We conducted a preliminary study to examine ortho-phthalate and replacement plasticizer concentrations in foods and food handling gloves from U.S. fast food restaurants. Methods We obtained hamburgers, fries, chicken nuggets, chicken burritos, cheese pizza (n = 64 food samples) and gloves (n = 3) from restaurants and analyzed them for 11 chemicals using gas chromatography mass spectrometry. Results We found DEHT at the highest concentrations in both foods (n = 19; median = 2510 µg/kg; max = 12,400 µg/kg) and gloves (n = 3; range: 28–37% by weight). We detected DnBP and DEHP in 81% and 70% of food samples, respectively. Median DEHT concentrations were significantly higher in burritos than hamburgers (6000 µg/kg vs. 2200 µg/kg; p < 0.0001); DEHT was not detected in fries. Cheese pizza had the lowest levels of most chemicals. Significance To our knowledge, these are the first measurements of DEHT in food. Our preliminary findings suggest that ortho-phthalates remain ubiquitous and replacement plasticizers may be abundant in fast food meals. Impact statement A selection of popular fast food items sampled in this study contain detectable levels of replacement plasticizers and concerning ortho-phthalates. In addition, food handling gloves contain replacement plasticizers, which may be a source of food contamination. These results, if confirmed, may inform individual and regulatory exposure reduction strategies.

Background Epistemological biases in environmental epidemiology prevent the full understanding of how racism’s societal impacts directly influence health outcomes. With the ability to focus on “place” and the totality of environmental exposures, environmental epidemiologists have an important opportunity to advance the field by proactively investigating the structural racist forces that drive disparities in health. Objective This commentary illustrates how environmental epidemiology has ignored racism for too long. Some examples from environmental health and male infertility are used to illustrate how failing to address racism neglects the health of entire populations. Discussion While research on environmental justice has attended to the structural sources of environmental racism, this work has not been fully integrated into the mainstream of environmental epidemiology. Epidemiology’s dominant paradigm that reduces race to a mere data point avoids the social dimensions of health and thus fails to improve population health for all. Failing to include populations who are Black, Indigenous, and people of color (BIPOC) in health research means researchers actually know very little about the effect of environmental contaminants on a range of population health outcomes. This commentary offers different practical solutions, such as naming racism in research, including BIPOC in leadership positions, mandating requirements for discussing “race”, conducting far more holistic analyses, increasing community participation in research, and improving racism training, to address the myriad of ways in which structural racism permeates environmental epidemiology questions, methods, results and impacts.

A decades-long decline in sperm counts in Western countries has coincided with an increase in obesity rates, prompting study into their association. Few of these studies have incorporated men of color, the sperm health of whom is relatively unknown. The present exploratory study evaluated the association between body mass index (BMI), race, ethnicity, and sperm parameters among a diverse sample of U.S. men attending a Washington, DC physician practice. Semen samples were collected and processed at a single laboratory and sperm concentration, motility, morphology, and count were evaluated according to World Health Organization (WHO) 5th edition criteria. Multivariate models accounted for covariates related to sperm health. The study population ( n = 128) was largely obese (45.3%) or overweight (34.4%), and 36.0% were black or Hispanic. Black men had lower adjusted sperm concentration compared to white men (75.0 million/mL to 107.4 million/mL, p = .01) and were more likely to have oligozoospermia ( p = .01), asthenozoospermia ( p = .004), and low sperm count ( p < .0001). Hispanic men had higher adjusted sperm concentration compared to non-Hispanic men (124.5 million/mL to 62.1 million/mL, p = .007) and were less likely to have teratozoospermia ( p = .001). Obesity and BMI were associated with lower sperm motility and count in crude models only. Given the study’s sample size its findings should be interpreted with caution but align with the limited epidemiological literature to date that has evaluated racial and ethnic differences in semen quality. Heightened clinical research attention is needed to ensure men of color are included in representative numbers in studies of urologic and andrologic health.