Last data update: May 13, 2024. (Total: 46773 publications since 2009)
Records 1-2 (of 2 Records) |
Query Trace: Straetemans M[original query] |
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Fentanyl-associated fatalities among illicit drug users in Wayne County, Michigan (July 2005-May 2006)
Algren DA , Monteilh CP , Punja M , Schier JG , Belson M , Hepler BR , Schmidt CJ , Miller CE , Patel M , Paulozzi LJ , Straetemans M , Rubin C . J Med Toxicol 2013 9 (1) 106-15 BACKGROUND: During the summer of 2005, multiple cities in the United States began to report outbreaks of fentanyl-associated fatalities among illicit drug users. The objectives of this study were to (1) determine if an outbreak of fentanyl-associated fatalities occurred in mid-2005 to mid-2006 and (2) to examine trends and compare features of fentanyl-contaminated heroin-associated fatalities (FHFs) with non-fentanyl, heroin-associated fatalities (NFHFs) among illicit drug users. METHODS: Baseline prevalence of fentanyl- and heroin-associated deaths was estimated from January to May 2005 based on recorded cause of death (determined by the medical examiner (ME)) using the Wayne County, MI, USA toxicology database. The database was then queried for both FHFs and NFHFs between July 1, 2005 and May 12, 2006. A FHF was defined as having fentanyl or norfentanyl (metabolite) detected in any postmortem biological sample and either (1) detection of heroin or its metabolite (6-acetylmorphine) and/or cocaine or its metabolite (benzoylecgonine) in a postmortem biological specimen or (2) confirmation of fentanyl abuse as the cause of death by the ME or a medical history available sufficient enough to exclude prescription fentanyl or other therapeutic opioid use. A NFHF was defined as detection of heroin, 6-acetylmorphine (heroin metabolite) or morphine in any postmortem biological specimen, heroin overdose listed as the cause of death by the ME, and absence of fentanyl detection on postmortem laboratory testing. Information was systematically collected, trended for each group and then compared between the two groups with regard to demographic, exposure, autopsy, and toxicology data. Logistic regression was performed using SAS v 9.1 examining the effects of age, gender, and marital status with fentanyl group status. RESULTS: Monthly prevalence of fentanyl-associated fatalities among illicit drug users increased from an average of two in early 2005 to a peak of 24 in May, 2006. In total, 101 FHFs and 90 NFHFs were analyzed. The median age of decedents was 46 and 45 years for the fentanyl and non-fentanyl groups, respectively. Fentanyl-contaminated heroin-associated fatalities (FHFs) were more likely to be female (p = 0.003). Women aged over 44 years (OR = 4.67;95 % CI = 1.29-16.96) and divorced/widowed women (OR = 14.18;95 % CI = 1.59-127.01) were more likely to be FHFs when compared to women aged less than 44 years and single, respectively. A significant interaction occurred between gender and age, and gender and marital status. Most FHFs had central (heart) blood samples available for fentanyl testing (n = 96; 95 %): fentanyl was detected in most (n = 91; 95 %). Of these, close to half had no detectable heroin (or 6-acetylmorphine) concentrations (n = 37; 40.7 %). About half of these samples had detectable cocaine concentrations (n = 20; 54 %). Median fentanyl concentration in central blood samples was 0.02 mcg/ml (n = 91, range <0.002-0.051 mcg/ml) and 0.02 mcg/ml (n = 32, range <0.004-0.069 mcg/ml) in peripheral blood samples. The geometric mean of the ratio of central to peripheral values was 2.10 (median C/P = 1.75). At autopsy, pulmonary edema was the most frequently encountered finding for both groups (77 %). CONCLUSION: Illicit drugs may contain undeclared ingredients that may increase the likelihood of fatality in users. Gender differences in fentanyl-related mortality may be modified by age and/or marital status. These findings may help inform public health and prevention activities if fatalities associated with fentanyl-contaminated illicit drugs reoccur. |
Comprehensive assessment of maize aflatoxin levels in Eastern Kenya, 2005 - 2007
Daniel JH , Lewis LW , Redwood YA , Kieszak S , Breiman RF , Flanders WD , Bell C , Mwihia J , Ogana G , Likimani S , Straetemans M , McGeehin MA . Environ Health Perspect 2011 119 (12) 1794-9 BACKGROUND: Aflatoxin, a potent fungal toxin, contaminates 25% of crops worldwide. Since 2004, 477 aflatoxin poisonings associated with eating contaminated maize have been documented in Eastern Kenya, with a case-fatality rate of 40%. OBJECTIVE: To characterize maize aflatoxin contamination during the high risk season (April-June) following the major harvests in 2005, 2006 (aflatoxicosis outbreak years), and 2007 (a non-outbreak year). METHODS: Households were randomly selected each year from the region in Kenya where outbreaks have consistently occurred. At each household, we obtained at least one maize sample (n = 716) for aflatoxin analysis using immunoaffinity methods and administered a questionnaire to determine the source (i.e. homegrown, purchased or relief) and amount of maize in the household. RESULTS: During outbreak years-2005 and 2006, 41% and 51% of maize samples respectively, had aflatoxin levels above the 20 ppb Kenyan regulatory limit for aflatoxin in grains for human consumption. In 2007 (non-outbreak year), 16% of samples were above the 20 ppb limit. In addition, geometric mean (GM) aflatoxin levels were significantly higher in 2005 (GM=12.92, max=48,000 ppb) and 2006 (GM=26.03, max=24,400 ppb) compared to 2007 (GM=1.95, max=2,500 ppb) (p value<.001). In all three years combined, maize aflatoxin levels were significantly higher in homegrown maize (GM=17.96) when compared to purchased maize (GM=3.64) or relief maize (GM=0.73) (p value<.0001). CONCLUSIONS: Aflatoxin contamination is extreme within this region and homegrown maize is the primary source of contamination. Prevention measures should focus on reducing homegrown maize contamination at the household level to avert future outbreaks. |
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