By contrast, it could reflect the increased prevalence of DM with age and the ability to detect an association with a lesser sample size when there is a greater cohort at risk for DM. The possible association of light marijuana use with decreased DM is similar to that of alcohol on DM and the metabolic syndrome, in which mild alcohol use was associated with lower prevalence of DM and the metabolic syndrome,and higher alcohol use associated with higher prevalence of DM and the metabolic syndrome.Smit and Crespo9 used the NHANES III population to examine dietary factors of non-marijuana users and marijuana users among adults aged 20e59 years. Similar to our data, they found that 45% reported used marijuana in their lifetime and 8.7% used marijuana in the past month. Current marijuana users had higher intakes of energy and nutrients and consumed more soft drinks but had slightly lower BMI than non-current marijuana users. Thus, it is unlikely that a healthier diet contributed to the decreased prevalence of DM among marijuana users found in our study. In our study, all marijuana users had lower BMI than non-users, with heavy marijuana users having the lowest BMI. The lower BMI may be protective for DM,indoor plant table although when we controlled for BMI, the prevalence of DM was not significantly changed suggesting additional BMI-independent pathways. Smit and Crespo did not record glycaemic parameters or prevalence of DM.
Using NHANES III data, marijuana users had lower rates of obesity and lower mean BMI, with current heavy marijuana users having the lowest BMI, in agreement with a recent report using National Epidemiologic Survey on Alcohol and the National Comorbidity Surveye Replication databases.Correcting for the effect of BMI, the association between marijuana use and DM was reduced by 17% but remained highly significant. We postulate that the decreased prevalence of DM and marijuana use may be due to the anti-inflammatory properties of marijuana. CBs found in marijuana favourably modify inflammation probably through the inhibitory actions on prostaglandins and COX-2.Hu and colleagues2 reported that CRP, but not interleukin-6 and tumour necrosis factor-a receptor-2, was associated with the risk of developing DM. In our study, serum level of CRP, fibrinogen ferritin, uric acid and WBC counts revealed varied associations with marijuana use. Of note, the CRP assay used in NHANES III was not a highly sensitive assay and is unlikely to pick up small changes in an inflammatory state in a single individual; however, it is still a robust measure of inflammation and is useful in population studies.However, we did find a U-shaped association between the CRP levels and marijuana use groups. Rodent studies using CBs have shown significant benefits against diabetic complications and atherosclerosis.Additionally, lower doses of CBs appear to be anti-inflammatory in rodents.CBs, including the non-psychoactive cannabidiol, have also been shown to attenuate progression of type 1 DM in animal models.We have not identified any study in human subjects or animals examining marijuana or its active ingredients and the incidence of type 2 DM, although one study found similar glucose levels in marijuana users as non-users.
In a prospective study using a cannabis based medicinal extract compared to placebo to treat diabetic neuropathy, glycaemic indices were not mentioned.We examined physical activity in patients using marijuana and found that it did not confound the association between marijuana and DM. Although the CB1 antagonist, rimonabant has been used successfully to treat DM,we are not surprised at the association between marijuana use and decreased prevalence of DM. Marijuana contains a variety of CBs, of which some, such as cannabidiol and delta9- tetrahydrocannabivarin, have antagonist properties that may mediate the anti-inflammatory properties of marijuana.A limitation of our study was its cross-sectional nature. Despite the efforts of NHANES to enrol a random representative sample of the US population, persons attending the study visits may differ from those not attending in subtle ways that may affect the results of this study. We are unable to conclude that marijuana use does not lead to DM nor do we suggest that marijuana should be a treatment for DM. Although we controlled for major confounders, it is possible that non-marijuana users and subjects with DM share some, as yet unknown, characteristic accounting for the relationship between DM and non-marijuana use. An additional limitation is that the marijuana use was based on self-report and self-report of illicit substances is often underestimated on self-reports.Self-report is subjected to recall bias. However, we expect that recall bias would be similar in those with DM as those without DM and would be unlikely to bias our results.
Although current marijuana users were divided into heavy and light users based on the number of times they reported using marijuana per month, the amount of marijuana consumed, route of consumption , duration of use and time when they quit were not reported. A potential limitation was that most patients with DM were identified by self-report, with a smaller number of patients identified by having an elevated fasting blood glucose levels. Because some patients with DM receiving treatment are euglycaemic, blood glucose levels alone cannot be used to identify those patients with DM. However, the percentage of marijuana user was similar in those patients with DM identified by self-report as that of those with DM identified by fasting glucose testing. While we analysed all patients with DM together, we estimated that over 98% of the patients had type 2 DM, and therefore, our results are likely to apply only to patients with type 2 DM. Another limitation is the possibility of a cohort effect since those who use marijuana may have other factors that may predispose decreased prevalence of diabetes compared to non-users besides lower BMI. In conclusion, marijuana use was associated with a decreased prevalence of DM. Prospective studies in rodents and humans are needed to determine a potential causal relationship between cannabinoid receptor activation and DM. Until those studies are performed, we do not advocate the use of marijuana in patients at risk for DM.Current practices vary around the world, so interviews were conducted with experts to gather the latest approaches. Several trends were apparent: odor limits based on number of dilutions are ineffective,plant growing stand working directly with the complainant to verify that an odor is present and then tracing it to the source is the first line of inquiry, and lengthy lists or scales of odor descriptors are unnecessary for initial investigations. When further investigation is required, due to overlapping odor sources or ongoing complaints, the steps of traditional risk assessment apply . Unlike the exposure and risk assessment of conventional air pollutants, the human sense of smell can be used as a detector by the air inspector or a trained panel. Analytical instruments then confirm or further explore the exposure to individual odorant compounds. The hazards from odor exposure, including both irritation and smell, are usually headache or nausea but also can include stress and emotional responses. Dose response relationships pass through several thresholds, the most commonly used being the odordetection threshold for 50% of a sensory panel . In addition, acute and chronic health hazard thresholds for odorants and odorless co-pollutants can be applied to air monitoring results, as demonstrated by several case studies.
For complex or unresolved odor exposures, sensory methods such as the Odor Profile Method have identified culprit odorants using an odor wheel, panel assessment of the intensity of the odor, and location information to identify the odor source. Confirmation is provided by analytical techniques, such as gas chromatography with a sensory port and parallel mass spectrometry. The promise of electronic noses that mimic the human sense of smell remains allusive, often failing to perform as well in the field as in the laboratory. The current path forward for environmental odor exposure assessment includes population-based metrics of odor, such as odor diaries and plume monitoring by panels, confirmed by modern analytical techniques.Air quality throughout the United States has improved greatly over the past 50 years , including in California . Nuisance odor complaints, however, continue to occupy a substantial portion of an air quality inspector’s duties. Such complaints range from minor annoyance to more substantial impacts on health and well being. More than half of the complaints received by air pollution agencies worldwide concern malodors , which holds true as well for the United States and California . Responding to odor complaints, however, is full of complexities. An odorous emission is typically a mixture of volatile chemicals rather than a single, easily identified compound. Even when present only at trace concentrations, most volatile emissions remain above their sensory thresholds and have the potential to adversely impact nearby communities . As a further complexity, the variability in odor perception and interpretation can be vexing to scientific approaches that seek to quantify, and thereby set limits for, any such nuisance. What is intolerable to one person can go unnoticed by another. Not surprising, both physiological and psychological factors, such as personality and risk aversiveness, come to bear with odor perception . Our sense of smell is constantly sampling the environment and assessing its quality. To this end, the olfactory system requires more of our genetic code than any other sense . Unpleasant odors act as warnings to avoid the odor source, such as spoiled food. Continual signaling can lead to the public’s concerns that the air is “unhealthy.” The hedonic signals, however, can be misleading, and some odorless compounds are deadly . Further, some people have no sense of smell , so they must rely on other senses instead. Residents often have economic concerns, too. The proximity of industry to their homes can have a negative impact on property values. For example, housing near wastewater treatment plants has been reported to be up to 15% lower in value . The residents’ well being and ability to have visitors at their home may be impacted as well.Although these industries are varied, common approaches to odor management have been employed, as have common approaches to nuisance odor investigations. Three factors that make odors a nuisance are evaluated: the description of the odor , the intensity of the odor, and the frequency and duration of its occurrence at the fenceline or within the neighborhood . Although odor notes and intensities are often reported by the public in vague terms, recruited panelists can be trained to provide more objective evaluations that involve common vocabulary and scaling. The three factors, in conjunction with meteorological data, can be used to identify the source of the odor, especially if the typical odorants emitted by the offending source are already known. If the source is unknown, ambiguous or overlapping with other sources, a more sophisticated investigation is required. Odor hedonic tone is a fourth factor that has been incorporated into national standards , considered by some to be more important than odor intensity , dismissed by others as too subjective, or sometimes considered already inherent in any odor complaint. Muñoz et al. observed that “odor measurement is often approached from very independent and disconnected research fields.” Both sensory and instrument measurements may be used that involve analytical chemistry, psychology, public health and hybrids thereof. Approaches from around the world vary in complexity, focus and regulatory aims and enjoy varying degrees of success . Merely identifying a subset of compounds in air does not indicate which are contributing to the odor problem. The odor description , intensity, and frequency plus duration of its occurrence need to be understood to identify the odor source and corrective actions. The odor offensiveness can assist certain cases as well. Risk assessment, the systematic evaluation of risks posed by exposures to chemicals and other stressors, has many of the same challenges as odor investigation. Both follow the source release-pathway-receptor conceptual model and employ many of the same analytical techniques . Both also suffer from large variability of uncertainties in their results, which can span an order of magnitude or more. Previous attempts to apply risk assessment to odor investigation have been partially successful, for example the use of source pathway-receptor discussions and a subset of those components . Large efforts over decades have refined the concepts and conventions used in risk assessment, particularly for pesticides, hazardous waste site cleanup and industrial chemicals management.