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Though exposure to the obesogen bisphenol A (BPA) is decreasing, a new study has linked substitute chemicals bisphenol S (BPS) and bisphenol F (BPF) to obesity as well.
“The potential health effects of BPS and other BPA replacement compounds should be monitored going forward, given that human exposure to these compounds is likely to continue to increase in the future,” wrote Melanie H. Jacobson, PhD, of New York University, and coauthors. Their report is in the Journal of the Endocrine Society.
BPA is one of the best known synthetic chemical obesogens, the authors noted. “It enlarges adipocytes and enhances differentiation from mesenchymal cells to adipocytes, inhibits adiponectin function, and is a synthetic estrogen and thereby can have sex-specific effects on body mass,” they explained.
To determine if the BPA analogues, BPS and BPF, could also induce obesity, the researchers analyzed data from 1,831 children and adolescents gathered through the U.S. National Health and Nutrition Examination Surveys from 2013 to 2016. Concentrations of BPA, BPS, and BPF were measured in spot urine samples and they were detected in 97.5%, 87.8%, and 55.2% of samples, respectively.
Log-transformed BPS concentrations were associated with an increased prevalence of general obesity (odds ratio, 1.16; 95% confidence interval, 1.02-1.32), which was defined as being greater than or equal to the 95th percentile of standardized body mass index z scores. BPS concentrations were also associated with an increased prevalence of abdominal obesity (OR, 1.13; 95% CI, 1.02-1.27), as was BPF detection (OR, 1.29; 95% CI, 1.01-1.64).
BPA and total bisphenols were not significantly associated with general or abdominal obesity.
“Though tissue and animal studies of the replacements are lacking, [BPS and BPF] have shown estrogenic activity. Further, BPS has been shown to promote preadipocyte differentiation, raising the possibility that these BPA replacements may induce the same obesogenic effects in humans,” the authors wrote.
They acknowledged that their results should be interpreted cautiously, because they were not able to determine if exposure to bisphenols influences weight gain or if obese children are merely more exposed to those compounds. In addition, because BPS and BPF are metabolized rapidly, spot urine samples cannot accurately reflect long-term exposure levels. Finally, because a good deal of food and beverage packaging contains bisphenols, “those who consume more of these products are more likely to have higher exposure levels,” they wrote.
The study was funded by grants from the National Institutes of Environmental Health Sciences. The authors reported no conflicts of interest.
SOURCE: Jacobson MH et al. J Endocr Soc. 2019 Jul 25. doi: 10.1210/js.2019-00201.
Though exposure to the obesogen bisphenol A (BPA) is decreasing, a new study has linked substitute chemicals bisphenol S (BPS) and bisphenol F (BPF) to obesity as well.
“The potential health effects of BPS and other BPA replacement compounds should be monitored going forward, given that human exposure to these compounds is likely to continue to increase in the future,” wrote Melanie H. Jacobson, PhD, of New York University, and coauthors. Their report is in the Journal of the Endocrine Society.
BPA is one of the best known synthetic chemical obesogens, the authors noted. “It enlarges adipocytes and enhances differentiation from mesenchymal cells to adipocytes, inhibits adiponectin function, and is a synthetic estrogen and thereby can have sex-specific effects on body mass,” they explained.
To determine if the BPA analogues, BPS and BPF, could also induce obesity, the researchers analyzed data from 1,831 children and adolescents gathered through the U.S. National Health and Nutrition Examination Surveys from 2013 to 2016. Concentrations of BPA, BPS, and BPF were measured in spot urine samples and they were detected in 97.5%, 87.8%, and 55.2% of samples, respectively.
Log-transformed BPS concentrations were associated with an increased prevalence of general obesity (odds ratio, 1.16; 95% confidence interval, 1.02-1.32), which was defined as being greater than or equal to the 95th percentile of standardized body mass index z scores. BPS concentrations were also associated with an increased prevalence of abdominal obesity (OR, 1.13; 95% CI, 1.02-1.27), as was BPF detection (OR, 1.29; 95% CI, 1.01-1.64).
BPA and total bisphenols were not significantly associated with general or abdominal obesity.
“Though tissue and animal studies of the replacements are lacking, [BPS and BPF] have shown estrogenic activity. Further, BPS has been shown to promote preadipocyte differentiation, raising the possibility that these BPA replacements may induce the same obesogenic effects in humans,” the authors wrote.
They acknowledged that their results should be interpreted cautiously, because they were not able to determine if exposure to bisphenols influences weight gain or if obese children are merely more exposed to those compounds. In addition, because BPS and BPF are metabolized rapidly, spot urine samples cannot accurately reflect long-term exposure levels. Finally, because a good deal of food and beverage packaging contains bisphenols, “those who consume more of these products are more likely to have higher exposure levels,” they wrote.
The study was funded by grants from the National Institutes of Environmental Health Sciences. The authors reported no conflicts of interest.
SOURCE: Jacobson MH et al. J Endocr Soc. 2019 Jul 25. doi: 10.1210/js.2019-00201.
Though exposure to the obesogen bisphenol A (BPA) is decreasing, a new study has linked substitute chemicals bisphenol S (BPS) and bisphenol F (BPF) to obesity as well.
“The potential health effects of BPS and other BPA replacement compounds should be monitored going forward, given that human exposure to these compounds is likely to continue to increase in the future,” wrote Melanie H. Jacobson, PhD, of New York University, and coauthors. Their report is in the Journal of the Endocrine Society.
BPA is one of the best known synthetic chemical obesogens, the authors noted. “It enlarges adipocytes and enhances differentiation from mesenchymal cells to adipocytes, inhibits adiponectin function, and is a synthetic estrogen and thereby can have sex-specific effects on body mass,” they explained.
To determine if the BPA analogues, BPS and BPF, could also induce obesity, the researchers analyzed data from 1,831 children and adolescents gathered through the U.S. National Health and Nutrition Examination Surveys from 2013 to 2016. Concentrations of BPA, BPS, and BPF were measured in spot urine samples and they were detected in 97.5%, 87.8%, and 55.2% of samples, respectively.
Log-transformed BPS concentrations were associated with an increased prevalence of general obesity (odds ratio, 1.16; 95% confidence interval, 1.02-1.32), which was defined as being greater than or equal to the 95th percentile of standardized body mass index z scores. BPS concentrations were also associated with an increased prevalence of abdominal obesity (OR, 1.13; 95% CI, 1.02-1.27), as was BPF detection (OR, 1.29; 95% CI, 1.01-1.64).
BPA and total bisphenols were not significantly associated with general or abdominal obesity.
“Though tissue and animal studies of the replacements are lacking, [BPS and BPF] have shown estrogenic activity. Further, BPS has been shown to promote preadipocyte differentiation, raising the possibility that these BPA replacements may induce the same obesogenic effects in humans,” the authors wrote.
They acknowledged that their results should be interpreted cautiously, because they were not able to determine if exposure to bisphenols influences weight gain or if obese children are merely more exposed to those compounds. In addition, because BPS and BPF are metabolized rapidly, spot urine samples cannot accurately reflect long-term exposure levels. Finally, because a good deal of food and beverage packaging contains bisphenols, “those who consume more of these products are more likely to have higher exposure levels,” they wrote.
The study was funded by grants from the National Institutes of Environmental Health Sciences. The authors reported no conflicts of interest.
SOURCE: Jacobson MH et al. J Endocr Soc. 2019 Jul 25. doi: 10.1210/js.2019-00201.
FROM JOURNAL OF THE ENDOCRINE SOCIETY