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Heavy drinkers also had more BOLD response compared to controls in the left VMPFC during anticipation

Relevant covariates thought to affect risk-taking performance and self-report of risk-taking were entered as covariates on Block 1 of the regression analyses. These included: age, family history of alcoholism, average # of alcoholic drinks per month, # of binge episodes in the prior 3 months, # of days/month of cannabis use in prior 3 months. BOLD response signal change variables for each ROI were entered on Block 2. The R 2 ∆ for the second step represented the degree to which BOLD activation was associated with baseline risk-taking performance or self-report of risk taking behavior, above and beyond the covariates listed in Step 1. There were a total of 28 tests run for Hypothesis 3 . Alpha was set at 0.05 for each test, as this was the first fMRI study of risk-taking in adolescent alcohol users and the analyses for Hypothesis 3 were considered exploratory. However, it should be noted that the probability of Type I error is increased due to the large number of tests that were run. The goals of this study were to use fMRI to: identify brain regions where neural activation associated with three separate stages of risky decision-making differed between heavy drinking adolescents and controls; examine whether neural activity associated with risky decision-making changed across a five-week period of abstinence and whether the trajectory of change over time differed for heavy drinkers vs. controls; and determine whether neural activation in regions showing baseline group differences during risky decision-making could predict differences in neuropsychological functioning , risk-taking performance, or self-report of risk taking behavior and impulsivity. Both ROI and whole-brain analyses were conducted to examine neural functioning in brain regions expected to activate during risky decision making as well as brain regions not implicated as fundamental, but which may still be relevant. With regard to group differences in neural activation patterns in ROIs at baseline ,grow systems for weed heavy drinkers showed less BOLD response relative to controls in the right insula during the anticipation phase of decision-making when previous balloon trials had popped.

Although it was originally hypothesized that heavy drinking adolescents would show increased activation in the insula during this stage of decision-making, the finding of reduced activation fits with previous investigations that suggest the insula is primarily involved in the experience of loss avoidance . With this interpretation, it may be that heavy drinkers were less concerned with avoiding further losses than controls, even when faced with a reminder of loss from the previous trial. During the experience of negative outcome evaluation , heavy drinkers showed increased activation in bilateral regions of the VMPFC compared to nondrinkers. This result is consistent with expectation given the widely replicated findings outlining the VMPFC as central to reward processing . Specifically, studies have suggested that the VMPFC is involved in encoding the reward value of a choice , with greater activation associated with appraisals of a higher valued item or result . While it was expected that heavy drinkers would show increased activation in the VMPFC relative to controls during evaluation of both “win” and “loss” outcomes, this effect was only observed during the evaluation of “loss” outcomes. Thus, it is possible that heavy drinkers and controls experience “winning” similarly; however, heavy drinkers may be less affected by negative outcomes, finding them more rewarding. This explanation is consistent with findings from Bogg and colleagues’ study, in which participants with greater recent alcohol consumption showed greater medial prefrontal cortex activity while experiencing outcomes achieved through riskier behavior . With regard to changes in BOLD activation during the stages of risky decision making across the five-week period of abstinence , findings were mixed. In brain regions where differences in BOLD activation were observed at baseline , no between-group differences were evident after two to three weeks of abstinence. This pattern of change was anticipated, though group differences were not expected to be non-significant until the third time point . However, the observed pattern is consistent with results of the preliminary study by Pulido and colleagues , in which baseline BOLD activation differences between heavy drinkers and controls to an alcohol cue reactivity task were non-existent in most brain regions after two to three weeks of abstinence. On the other hand, some surprising group differences in the trajectory of BOLD response to risky decision-making across the five-week abstinence period were seen.

Specifically, controls showed increasing activation over time in the right anterior cingulate during the pre-response assessment phase of decision-making, while heavy drinkers did not show changes over time in this region during this phase of decision-making. Instead, heavy drinkers showed increasing activation over time in the right ventromedial prefrontal cortex/anterior cingulate during the anticipation phase of decision-making, while controls did not show this change. The anterior cingulate has been linked with a variety of separate functions at different stages in the decision-making process. Specifically, during the pre-response assessment phase of decision-making, it has been shown to have a primary role in cognitive control processes such as error and performance monitoring . During anticipation of reward and reward evaluation, the anterior cingulate has also shown high reactivity, particularly when there is a higher degree of effort that must be undertaken to “earn” a reward . Other studies have suggested that, like the insula, the anterior cingulate is associated with loss aversion during the anticipation of risks, with greater activation observed as the probability of a negative outcome increases . Thus, increasing BOLD response in the anterior cingulate over time during the pre-response assessment phase may be indicative of learning, or an increased attention to cognitive strategies for optimal performance on the task as participants become increasingly comfortable with the task format. As controls showed this pattern but heavy drinkers did not, it is possible that heavy drinkers did not increase attention to cognitive strategies/performance monitoring over repeated assessments to the same degree as controls. Similarly, increased BOLD response in the VMPFC/anterior cingulate during the anticipation phase of decision-making may be indicative of increasing loss aversion or greater attention to the probability of loss with increasing abstinence. As the heavy drinkers showed this pattern but controls did not, this suggests that alcohol may alter brain functioning in regions responsible for aversion to loss which in turn, could contribute to greater risk taking; in addition, short-term abstinence may contribute to neural recovery in these regions. Other regions of the brain demonstrated main effects of group on BOLD response averaged across time points, indicating that some neural functioning differences between heavy drinkers and controls persisted across the abstinence period. Specifically, heavy drinkers had less BOLD response relative to controls in bilateral regions of the DLPFC during the pre-response assessment phase of the task , in the left insula during anticipation , and in the right VMPFC during anticipation .

The finding that heavy drinkers exhibited hyporeactivity relative to controls in the DLPFC during pre-response assessment is consistent with expectation as well as with previous studies indicating that adolescents engage the DLPFC to a lesser extent than do adults during risky decision-making . In addition,cannabis indoor grow system hypore activity in widespread brain regions during a risky decision-making task has been observed in a sample of adolescent males with substance use problems who had been abstinent from substances for at least 30 days. It is important to note that all adolescents in this sample had comorbid conduct disorder, so it is impossible to determine whether the observed neural abnormalities resulted from substance use, psychiatric factors, or both. The finding that heavy drinkers displayed decreased left insular activity averaged across time points during anticipation is consistent with between-group differences in baseline BOLD response observed in this study, where heavy drinkers showed decreased right insular activity during anticipation, when previous balloons had popped. However, it is interesting that differences in right insular activity did not persist across the abstinence period as is observed in the left insula. This may be because the left insular activity was observed after previous “winning” trials while the right insular activity was observed after previous “loss” trials . If insular activity represents a marker for loss aversion, it may be that loss aversion is triggered more quickly when the memory of loss is more salient. In other words, heavy drinkers may continue to be less averse to loss during anticipation of an uncertain outcome when the memory of a recent reward is more salient. The finding that heavy drinkers showed increased left VMPFC activity averaged across time points during anticipation is consistent with the idea that adolescent heavy alcohol users may pay greater attention to the potential rewarding properties of an uncertain outcome compared to nondrinkers. This interpretation also fits with the possibility that alcohol use may alter neural functioning patterns related to reward sensitivity, and that these alterations may persist for longer periods than do alterations related to loss aversion. However, the finding that controls had greater BOLD response than heavy drinkers averaged across time in the right VMPFC during anticipation is somewhat surprising as we might expect the opposite pattern. With regard to baseline BOLD response as a predictor of executive functioning, risk-taking task performance, and self-report of risk-taking and impulsive behavior , baseline BOLD response during risky decision-making was not associated with executive functioning performance or performance on the risk-taking task.

However, greater activation in the VMPFC during negative outcome evaluation was predictive of self-report of greater risk-taking in the naturalistic environment. This is consistent with other studies that have reported similar relationships between BOLD response and ratings of risk-taking in adolescents. For example, Galvan and colleagues found that BOLD response in the nucleus accumbens during a reward processing task was positively correlated with adolescents’ ratings of both the likelihood of engaging in risky behaviors in the near future and ratings of anticipated positive consequences as a result of such risky behavior. Nucleus accumbens activity was negatively correlated with ratings of anticipated negative consequences of risky behavior. Findings from the exploratory whole-brain analysis suggest that heavy drinkers and controls may show differential neural response to risky decision-making in regions not identified as ROIs. During the baseline anticipation phase, heavy drinkers showed less BOLD response than controls in the right middle frontal gyrus and left anterior cingulate . During the baseline outcome evaluation phase, heavy drinkers showed greater BOLD response than controls in bilateral middle temporal and cingulate gyrus, right supramarginal gyrus, inferior/medial/superior frontal, and precentral gyrus areas. These baseline group differences were not evident after two to three weeks of abstinence, except for the right middle frontal gyrus during anticipation, where BOLD response was greater for controls, averaged across time points. During the pre-response assessment phase of decision-making, controls showed greater BOLD response than heavy drinkers averaged across time points, in widespread regions including bilateral medial temporal, inferior parietal, inferior/middle/medial frontal, anterior cingulate, right thalamus, and right superior frontal areas. In contrast, during the anticipation phase, heavy drinkers showed more BOLD response relative to controls averaged across time points in bilateral cingulate cortices, middle/inferior frontal regions, and occipital areas. During outcome evaluation, heavy drinkers showed greater BOLD response relative to controls averaged across time points in bilateral inferior/middle/medial frontal, right inferior parietal, right superior temporal, left occipital, and left thalamic regions. Overall, results of the whole brain analysis provide evidence that there are other regions implicated in the stages of risky decision-making, which show neural functioning differences between heavy drinkers and controls. Some neural functioning differences in these areas appear to resolve after two to three weeks of abstinence, while others persist for at least 4+ weeks. Some limitations should be mentioned. First, among the heavy drinking adolescents, there was considerable variability in the reported length of abstinence from alcohol prior to entering the study. Although the ideal length of abstinence at study entrance was between 4-10 days, some subjects reported much longer periods of abstinence , while others reported shorter periods . Although the mean number of days of reported abstinence in the heavy drinking group was consistent with the ideal length of abstinence it is possible that the variability may have skewed the results.

The greatest increase in product formation was seen when the reactants originated indoors

Occupational exposure to VOCs and formaldehyde are associated with some of the samesymptoms as SBS . However, levels of these compounds in office and other buildings are considerably lower than those found in industrial settings. Concentrations of total VOC in office buildings commonly range between less than 100 µg/m3 and several thousand micrograms per cubic meter, but maximum values of up to 50,000 µg/m3 have been reported . More than 350 VOCs have been detected at concentrations exceeding 1 ppb in indoor air , but generally only about 30 to 70 are routinely measured and even fewer are consistently detected in a majority of office buildings . When a group of Nordic scientists reviewed the literature up to early 1996 regarding VOC/ TVOC and health, they concluded that neither exposure nor epidemiological studies provided conclusive evidence that TVOC provided a risk index for health and comfort effects in buildings . A similar conclusion was reached in a review of studies that examined the association between SBS symptoms and indoor airborne PM, to which VOC can be adsorbed . However, the Nordic scientists stated that indoor air pollution, including VOCs, was most likely causally linked to effects on health and comfort. They also emphasized that there were “problems of principle with the concept of TVOC as such” because it is poorly defined— that is, it refers to different mixtures of chemicals with varying biological effects and is used in an unsystematic manner. Additionally, the use of various different sampling and analytical methods constitutes a major source of variability between studies . There are various other problems with the way current assessments of factors related to SBS symptoms are conducted. Measurements are often taken in only a few locations in a building, without accounting for the fact that there are microclimates in buildings resulting from differences in the ventilation rates,cannabis grow supplier in the number of occupants and the amount of bio-effluents they produce, and in the furnishing and equipment and, therefore, in the sources of chemical compounds and their source strength.

Additionally, symptoms are generally assessed via questionnaires, and these differ between studies and are not always validated. The period for which symptoms are assessed also varies from the single day on which environmental measurements are taken to as long as the previous year. In several studies, there is a considerable lapse of time between these measurements and the assessment of symptoms. The number and type of factors included as covariates or confounders in the statistical analysis also varies substantially between studies. Additionally, none of the available studies that we reviewed accounted for the fact that people are exposed to a wide variety of chemicals in micro-environments other than the workplace—particularly at home, where they spend the majority of their time. These considerations may explain the frequent failure to detect an association between VOC/TVOC and SBS. Various other hypotheses have been proposed to explain why VOCs may be an important factor in SBS, although the evidence is inconclusive . For example, it is possible that SBS is associated with a subgroup or subgroups of VOCs rather than TVOC and/or with intermediates or products of reactions between certain types of VOCs and ozone or various reactive oxygen and nitrogen species. Principal component analysis has become an important tool for identifying groups of chemicals and other factors that could explain the different frequencies of SBS symptoms in different buildings. It condenses a set of highly correlated variables into a smaller number of linearized sums . This works particularly well for VOCs because subsets of them have common sources. Because VOCs can originate from more than one source, they can be associated with more than one PC. PCA on a total of 39 VOCs measured in 12 California office buildings was used to identify exposure metrics—that is, mathematical expressions of the potential or actual agent that causes an adverse health effect . The exposure metric termed irritancy/PC emerged as the most significant predictor of irritant symptoms.

It consisted of the two most relevant vectors obtained by PCA, which were identified as representing carpet and building material emissions and emissions from cleaning products and water-based paint; it also accounted for the irritancy of VOCs relative to toluene. When analyzed separately, the cleaning products and water-based paints source vector provided the most important symptom prediction, with statistically significant adjusted ORs ranging from 1.7 to 2.2 for eye, skin, throat, stuffy nose, and overall symptoms. Other studies that used PCA on VOCs, but without accounting for their irritancy, linked photocopier emissions to mucous membrane symptoms; paint-derived VOCs to sore throat symptoms; construction material emission to dry eyes, mucous membrane symptoms overall, and short breath; and VOCs associated with furniture coating to shortness of breath . A combination of PCA and partial least squares analysis of VOCs desorbed from dust samples from nine office buildings identified a set of compounds that could account for 80% of the variance in the frequency of mucous membrane complaints and another set of compounds that explained 66% of the variance in difficulty concentrating . The possibility that oxidative degradation products of α- or β- pinene were among the compounds associated with mucous membrane irritation was particularly intriguing. As discussed later, the oxidation of terpenes produces formaldehyde and other aldehydes, and there are indications that some considerably more irritating substances are also formed. PCA was also used to identify factors that would be able to distinguish buildings with a high prevalence of SBS symptoms from those with a low prevalence of SBS symptoms . The most complex model was able to separate 71% of high-prevalence from low-prevalence buildings, and the most important variable was the higher concentration or more frequent detection of compounds with higher retention times in gas chromatography analysis in buildings with a low prevalence of symptoms.In five office buildings with different frequencies of reported SBS symptoms, cluster analysis was used to identify “hot” and “cold” spots—that is, areas with high and low symptom frequencies—in each building . Only people working in areas where chemical and other measurements had been taken were included in the analysis.

The most striking finding was that the same factors were associated with different symptoms and the same symptoms were associated with different factors in the various buildings. Furthermore, a recent comparison of personal exposures to aldehydes, amines, NO2 , O3 , particles, and VOCs in eight office buildings in a town in northern Sweden found that intra-individual differences accounted for the variation of 78% of the 123 measured compounds, whereas differences among buildings were the major source of variability for only 14% of the compounds . This highlights the inadequacy of a few stationary measurements in buildings and underscores the need for personal exposure measurements. Weschler and Shields noted that the inability to identify irritants in an indoor setting does not mean that the setting is free of irritants but may simply reflect the difficulty or even impossibility to detect the relevant compound with the analytical techniques routinely used to monitor indoor air quality. It may not be the VOCs that cause SBS symptoms; rather, it may be reaction products,cannabis drainage system particularly the reaction of unsaturated VOCs with O3 and various oxygen and nitrogen radicals . The major source of O3 in indoor air is outdoor-to-indoor transport . Additionally, office equipment, such as laser printers and photocopiers, has been shown to emit not only VOC but also O3 . Monoterpenes are unsaturated VOCs that contain one or two double bonds that react readily with O3 , OH radicals, and nitrate radicals to yield various aldehydes, ketones, carboxylic acids, and organic nitrates . The reaction of terpenes at concentrations below their no observed effect level with O3 yielded reaction products that acted as strong airway irritants in an established mouse bio-assay . Although known irritants were among the reaction products, they did not fully account for the observed effect, suggesting that one or more highly irritating intermediates and/or as yet unidentified products were formed. A possible candidate is submicron particles, which have been shown to form when O3 reacts with terpenes under simulated office conditions . Modeling and experimental measurements demonstrated that the product formation of uni- and bimolecular reactions increased at decreasing ventilation rates, whether or not there was sufficient time for the system to achieve steady state .Therefore, the decrease in SBS symptom frequency observed with increasing ventilation rates is likely to reflect not only the removal of pollutants with indoor sources but the restriction of reactions among indoor pollutants. A study of 29 office buildings in northern Sweden is frequently cited to support the hypothesis that reaction products, rather than VOCs themselves, are associated with SBS symptoms . Compared with buildings where TVOCs were higher in the room air than in the intake air, buildings where VOCs were “lost” from intake to room air had an OR of 39 of being SBS buildings .

The more TVOCs were lost, the higher the concentration of formaldehyde was, providing indirect confirmation of prior experimental data and indicating that VOCs reacted with O3 to form various aldehydes, including formaldehyde . A major shortcoming of this study is that VOCs were measured up to 6 mo after SBS symptoms had been assessed by questionnaire. Furthermore, PCA of the data from the same 29 office buildings did not confirm the significant association of lost TVOCs with the prevalence of SBS symptoms . However, this may have been attributable to the simultaneous “loss” and “gain” of TVOCs in separate rooms within the same building. It is rather striking that investigations of the possible associations between VOCs and SBS have focused exclusively on VOCs at the workplace, although exposure occurs in almost all micro-environments—particularly at home, but also in cars, public transportation, restaurants, pubs, stores, and movie theaters . Although rather different half-lives of elimination have been reported for VOCs from blood, there is general agreement that VOCs are rapidly taken up and that their elimination is characterized by a two-exponential, and in some cases a three-exponential, equation . This suggests that blood VOCs are distributed to multiple tissues for storage and that the kinetics of elimination vary with the storage site. This is confirmed by measurements of VOCs in breath, which suggest that under steady state conditions, the residence times for bloodor liver, organs, muscle, and fat are approx 3 min, 30 min, 3 h, and 3 d, respectively . From these data, it appears possible that bio-accumulation occurs and, therefore, that not only the kinetics of VOC uptake and elimination but also the threshold for adverse health effects may differ after acute and chronic exposure. It remains to be established whether cumulative exposure to certain groups of VOCs is a better predictor of SBS symptoms than exposure in the work environment alone.In recent years, several environmental monitoring studies other than those attempting to identify factors involved in SBS symptoms have focused on VOC exposure. A major impetus for such studies was provided by the fact that several VOCs are among the 189 hazardous air pollutants listed in the US Clean Air Act Amendment. These include the known human carcinogens, benzene and 1,3-butadiene, and the probable human carcinogens, styrene, methylene chloride, and carbon tetrachloride. The International Agency for Research on Cancer also recently reclassified formaldehyde from Group 2A to Group 1 . Until recently, the majority of research on VOCs focused on identifying exposures in outdoor air, but data on indoor residential exposure to VOCs are beginning to accumulate . In studies measuring personal and residential indoor as well as outdoor concentrations of VOCs, personal exposure of adults and children generally exceeded residential indoor exposure by a substantial margin, and indoor concentrations were considerably higher than outdoor levels . An analysis of data on personal, residential indoor and outdoor, and work environment indoor concentrations of VOCs in Helsinki, Finland indicated that the geometric means of residential concentrations of VOCs exceeded those of work environments . Notably, the sample was representative of the population of Helsinki and included people with occupational exposures to VOCs, as indicated by the high maxima reported for the work environment, which were two orders of magnitude higher than mean residential concentrations.