A Preliminary Canadian Environmental Emissions Inventory for Endogenous and Retail Pharmaceutical Estrogens

ABSTRACT

Pharmaceuticals and personal care products (PPCPs), including estrogen pharmaceuticals, have been an environmental concern for well more than a decade, but no environmental emissions inventory for Canada has yet been published. Endogenous estrogens cannot be distinguished from the equivalent pharmaceutical estrogens in the environment. Therefore, data were compiled to estimate total environmental emissions of endogenous and retail pharmaceutical estrogens by the Canadian population for year 2007. Approximately 1,700 kg of pharmaceutical estrogens were dispensed through retail pharmacies in Canada in 2007. Of this amount, total environmental emissions were estimated to be approximately 730 kg, half to surface water via municipal sewage outfalls (> 90% via sewage treatment plants providing primary, secondary, or tertiary treatment), and half to the soil vadose zone and (potentially) groundwater via in situ sewage treatment systems. Approximately 960 kg of endogenous estrogens were excreted by the Canadian population, with about 420 kg reaching the environment, again approximately half to each of surface water and soil/groundwater. In situ sewage treatment may deliver an equivalent load of estrogens to the environment as do sewage treatment plants, despite servicing only 22% of the Canadian population.

Key Words:

• endogenous
• pharmaceutical
• estrogen
• emissions
• inventory
• Canada

ACKNOWLEDGMENTS

This study was funded entirely by Risklogic Scientific Services, Inc. The authors thank Brogan Inc. for providing summary data on prescription drug sales in Canada. The authors also thank Dr. Leonard Ritter, CNTC, University of Guelph, Guelph, ON, for comments offered on the draft manuscript.

Notes

¹Data from Statistics Canada (SC 2007), unless otherwise noted.

²As determined by Johnson and Williams (2004).

³As determined by Johnson et al. (2000); not reported by Johnson and Williams (2004).

⁴Data for females 13 to 50 years; excludes pregnant females; average age of menarche = 13 yrs (Anderson et al. 2003); average age of onset of menopause = 51 yrs (USNIA 2008; U.S. data assumed representative of Canada).

⁵Based on latest pregnancy rate data from Statistics Canada (SC 2004): pregnancy rate by age group, as a proportion of the population in that age group: < 15 yrs = 0.002; 15 to 19 yrs = 0.0305; 20 to 24 yrs = 0.0812; 25 to 29 yrs = 0.1196; 30 to 34 yrs = 0.1115; 35 to 39 yrs = 0.050; 40 to 49 yrs = 0.0108; ≥ 50 yrs = 0 (assumed).

⁶Primarily excreted during pregnancy (Sagawa 2006); value represents average across gestation period as excretion increases as gestation advances; average gestational period was assumed to be 266 days from date of conception.

⁷Data for females ≥ 51 years of age; average age of onset of menopause = 51 yrs (USNIA 2008; U.S. data assumed representative of Canada).

⁸Data for males ≥ 15 years of age; average age of puberty in males is approximately 2 years later than females (Marshall and Tanner 1986)

¹After van den Belt et al. (2004); average of multiple tests.

²After Sagawa (2006).

³After Metcalfe et al. (2001), Bovee et al. (2004); range given as number of tests limited.

⁴Assumes 75% degradation of influent estrogens.

⁵Assumes no degradation of influent estrogens.

¹Assumed; conjugated estrogens are mixtures of natural estrogens with undisclosed mixtures and proportions of individual hormones.

² Equivalent to estrone; estropipate is a salt of estrone and is metabolized to estrone for hormonal activity.

³After van den Belt et al. (2004); average of multiple tests; relative to 17β -estradiol.

⁴Metabolic longevity and hormonal activity in humans implies a potency of ethinylestradiol in humans of 100, relative to 17β -estradiol (Johnson and Williams 2004; Åtedt et al. 1979).

⁵After Sagawa (2006).

⁶After Bovee et al. (2004) and Hasenbrink et al. (2006); range given as number of tests limited.

⁷Mestranol is the 3-methyl ether of ethinylestradiol (EE2) and is hepatically metabolised (activated) to EE2; in humans, 1 unit of mestranol is pharmacokinetically equivalent to 0.7 units of ethinylestradiol (Faigle and Schenkel 1998), implying a potency of 70 in humans, relative to 17β -estradiol.

⁸Assumes 75% degradation of influent estrogens.

⁹ Assumes no degradation of influent estrogens.