Lead exposure, weight gain, hypertension, and early mortality: case study and review

Lead exposure, weight gain, hypertension, and early mortality: case study and review

Background:
As increased lead exposure from contaminated marijuana use in the USA and Germany has been confirmed, the potential impacts of severe or light lead exposure are being drawn once again into the public light. The mean adult lead exposure in the USA dropped by 41% from the 1990s to the 2000s from 2.76 μg/dL to 1.64 μg/dL, which has been causally shown to prevent the nearly triple the rate of kidney death and double the rate of peripheral artery disease, which includes cardiovascular death which was present before (Muntner). These low levels of increased lead exposure have been shown to result in a 1.55 increased odds ratio for mortality in all cardio-vascular mortality, after adjusting for all other factors (Menke). This translates into over 7 years of lost life expectancy (Tsai), simply from the cardio-vascular effects of lead toxicity.
The mean for previous mean lead exposure is now still extant in the higher quartile of adults now that lead exposure has dropped significantly, which makes what was formerly believed to be a safe level of lead exposure very dangerous for those who are still exposed to elevated levels of lead. The expected drop in hypertension from removal of lead from the environment within these boundaries is estimated at 17.5% (Pirkle). Hypertension is a condition which induces an increased hazard ratio of about 1.30 of at least one annual kilogram of weight gain (Stevens), or around 80 kilograms in a lifetime. These weight changes as well as lead exposure have been associated or identified causally with neurological changes, most notably brain lesions (Stewart), which brain imaging and cardiovascular data in this case study have confirmed.
Fortunately for this study and for those who are exposed to lead-infused marijuana or environmental hazards, a study from Veterans affairs has found that increased mortality and negative health effects from lead exposure is only significant with long-term cumulative exposure (Weisskopf). Because the trials were conducted over a period of multiple years, it is likely that there will not be long term or lasting effects once lesions are allowed to heal and with natural expiration of the toxin from the body.
Case study and Results:
Unfortunately, in the case study of a responsible adult marijuana user (5-10 grams at 10% mean THC content per week) in the Northeast of the USA, these sorts of statistical analyses were not useful. In the first run, diastolic blood pressure was over 95 directly after the trial though lead was not initially considered as a factor, with considerations of light alcohol use and high nicotine intake believed to be causally tied to this negative symptom. Re-trial, without regular use of nicotine (substitution of pipe tobacco, with virtually no absorbed nicotine for cigarette tobacco which has between 5 and 13 times the amount of absorbed nicotine) and no use of alcohol, determined lead levels of around 3.5 μg/dL, or levels qualifying as occupational hazard and outside of the range of environmental exposure. With levels taken only one month after the trial had ended and a half-life of lead in the human body of around one month, it can be assumed that these levels at a maximum were at least 7 μg/dL (Barbosa). The increases in blood pressure associated with occupational exposure to lead, which this level still falls into the highest decibel among, are around 10 mm Hg in blood pressure, though due to the young age and good health of the subject and lower expected peak exposure level symptoms may not be as exacerbated as noted in long-term occupational exposure ratios (Glenn).
Physical or cardio-vascular side effects aside, the exposure to lead also has multiple symptoms of neurodegeneration which present themselves and confound earlier attempts to pinpoint neurological effects of THC on the brain, though increased functional connectivity was still noted and remains a confirmed positive effect of marijuana on the brain. The impact of lead on the brain in any amounts on adults or children has been shown to be increased brain lesions and negative on all brain structures as proven using MRI technology (Stewart). This is consistent with the single photon emission computed tomography scan performed which showed increased functional connectivity, but altered blood-flow throughout the brain (Fischer), believed at the time to be the result of specific toxins, though now shown to be an undocumented variable: the environmental toxin lead.
Works Cited:
Barbosa Jr, Fernando, et al. “A critical review of biomarkers used for monitoring human exposure to lead: advantages, limitations, and future needs.”Environmental health perspectives (2005): 1669-1674.
Fischer, Paul Andreas. “Single Photon Emission Computed Tomography – Alcohol and Marijuana light use, case study.”http://platophilosphy.blogspot.com/2014/07/effects-of-regular-or-light-marijuana.html (2014).
Glenn, Barbara S., et al. “The longitudinal association of lead with blood pressure.” Epidemiology 14.1 (2003): 30-36.
Menke, Andy, et al. “Blood lead below 0.48 μmol/L (10 μg/dL) and mortality among US adults.” Circulation 114.13 (2006): 1388-1394.
Muntner, Paul, et al. “Continued decline in blood lead levels among adults in the United States: the National Health and Nutrition Examination Surveys.”Archives of Internal Medicine 165.18 (2005): 2155-2161.
Pirkle, James L., et al. “The relationship between blood lead levels and blood pressure and its cardiovascular risk implications.” American journal of epidemiology 121.2 (1985): 246-258.
Stevens, J., et al. “Associations between weight gain and incident hypertension in a bi-ethnic cohort: the Atherosclerosis Risk in Communities Study.”International journal of obesity and related metabolic disorders: journal of the International Association for the Study of Obesity 26.1 (2002): 58-64.
Stewart, W. F., et al. “Past adult lead exposure is linked to neurodegeneration measured by brain MRI.” Neurology 66.10 (2006): 1476-1484.
Tsai, Shan P., Robert J. Hardy, and C. P. Wen. “The standardized mortality ratio and life expectancy.” American journal of epidemiology 135.7 (1992): 824-831.
Weisskopf, Marc G., et al. “A prospective study of bone lead concentration and death from all causes, cardiovascular diseases, and cancer in the Department of Veterans Affairs Normative Aging Study.” Circulation 120.12 (2009): 1056-1064.
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