Aride Drugged Driving

[man of steel]

This is the worst thing I have ever seen!

I am on 2 scripts now that mimic me being a person on meth.

If I get pulled over is it going to take an hour or more to tell me I have Diabetes?

Lisinopril Sticker says can impare me.

Glimepiride May cause dizziness

No exposure to sun, I turned red from the sun METH

Am I supposed to get out of my car? Its sunny out

I am going to the rx to ask for counseling and a note from him explaining why I would fail the test.

I gave 3 yrs for this nation to get my blood, A cop does not have that right!

So I am red faced blood pressure out of control,Irregular pulse,bloodshot eyes from not sleeping

and have to worry about this?

I'll let you know what I am told.

I'm glad to see a cop can diagnose whats going on the Dr seems to be having issues.

State Police Post for free medical checkups?

 

 

The DRE protocol is a standardized and systematic method of examining a Driving Under the Influence of Drugs (DUID) suspect to determine the following: (1) whether or not the suspect is impaired; if so, (2) whether the impairment relates to drugs or a medical condition; and if drugs, (3) what category or combination of categories of drugs are the likely cause of the impairment. The process is systematic because it is based on a complete set of observable signs and symptoms that are known to be reliable indicators of drug impairment.

 

A DRE never reaches a conclusion based on any one element of the evaluation, but instead on the totality of facts that emerge. The DRE evaluation is standardized because it is conducted the same way, by every drug recognition expert, for every suspect whenever possible. Standardization is important because it makes the officers to be better observers, helps to avoid errors, and promotes professionalism.

 

The 12-Step DRE Protocol

The DREs utilize a 12-step process to assess their suspects:

 

1. Breath Alcohol Test

 

The arresting officer reviews the subject’s breath alcohol concentration (BrAC) test results and determines if the subject’s apparent impairment is consistent with the subject’s BrAC. If so, the officer will not normally call a DRE. If the impairment is not explained by the BrAC, the officer requests a DRE evaluation.

 

2. Interview of the Arresting Officer

 

The DRE begins the investigation by reviewing the BrAC test results and discussing the circumstances of the arrest with the arresting officer. The DRE asks about the subject’s behavior, appearance, and driving. The DRE also asks if the subject made any statements regarding drug use and if the arresting officer(s) found any other relevant evidence consistent with drug use.

 

3. Preliminary Examination and First Pulse

 

The DRE conducts a preliminary examination, in large part, to ascertain whether the subject may be suffering from an injury or other condition unrelated to drugs. Accordingly, the DRE asks the subject a series of standard questions relating to the subject’s health and recent ingestion of food, alcohol and drugs, including prescribed medications. The DRE observes the subject’s attitude, coordination, speech, breath and face. The DRE also determines if the subject’s pupils are of equal size and if the subject’s eyes can follow a moving stimulus and track equally. The DRE also looks for horizontal gaze nystagmus (HGN) and takes the subject’s pulse for the first of three times. The DRE takes each subject’s pulse three times to account for nervousness, check for consistency and determine if the subject is getting worse or better. If the DRE believes that the subject may be suffering from a significant medical condition, the DRE will seek medical assistance immediately. If the DRE believes that the subject’s condition is drug-related, the evaluation continues.

 

4. Eye Examination

 

The DRE examines the subject for HGN, vertical gaze Nystagmus (VGN) and a for a lack of ocular convergence. A subject lacks convergence if his eyes are unable to converge toward the bridge of his nose when a stimulus is moved inward. Depressants, inhalants, and dissociative anesthetics, the so-called "DID drugs", may cause HGN. In addition, the DID drugs may cause VGN when taken in higher doses for that individual. The DID drugs, as well as cannabis (marijuana), may also cause a lack of convergence.

 

5. Divided Attention Psychophysical Tests

 

The DRE administers four psychophysical tests: the Romberg Balance, the Walk and Turn, the One Leg Stand, and the Finger to Nose tests. The DRE can accurately determine if a subject’s psychomotor and/or divided attention skills are impaired by administering these tests.

 

6. Vital Signs and Second Pulse

 

The DRE takes the subject’s blood pressure, temperature and pulse. Some drug categories may elevate the vital signs. Others may lower them. Vital signs provide valuable evidence of the presence and influence of a variety of drugs.

 

7. Dark Room Examinations

 

The DRE estimates the subject’s pupil sizes under three different lighting conditions with a measuring device called a pupilometer. The device will assist the DRE in determining whether the subject’s pupils are dilated, constricted, or normal. Some drugs increase pupil size (dilate), while others may decrease (constrict) pupil size. The DRE also checks for the eyes’ reaction to light. Certain drugs may slow the eyes’ reaction to light. Finally, the DRE examines the subject’s nasal and oral cavities for signs of drug ingestion.

 

8. Examination for Muscle Tone

 

The DRE examines the subject’s skeletal muscle tone. Certain categories of drugs may cause the muscles to become rigid. Other categories may cause the muscles to become very loose and flaccid.

 

9. Check for Injection Sites and Third Pulse

 

The DRE examines the subject for injection sites, which may indicate recent use of certain types of drugs. The DRE also takes the subject’s pulse for the third and final time.

 

10. Subject’s Statements and Other Observations

 

The DRE typically reads Miranda, if not done so previously, and asks the subject a series of questions regarding the subject’s drug use.

 

11. Analysis and Opinions of the Evaluator

 

Based on the totality of the evaluation, the DRE forms an opinion as to whether or not the subject is impaired. If the DRE determines that the subject is impaired, the DRE will indicate what category or categories of drugs may have contributed to the subject’s impairment. The DRE bases these conclusions on his training and experience and the DRE Drug Symptomatology Matrix. While DREs use the drug matrix, they also rely heavily on their general training and experience.

 

12. Toxicological Examination

 

After completing the evaluation, the DRE normally requests a urine, blood and/or saliva sample from the subject for a toxicology lab analysis.

 

Nothing in or about the DRE protocol is new or novel. The DRE protocol is a compilation of tests that physicians have used for decades to identify and assess alcohol- and/or drug-induced impairment.

 

 

 

Three determinations of a DRE

A DRE conducts a detailed, diagnostic examination of persons arrested or suspected of drug-impaired driving or similar offenses. Based on the results of the drug evaluation, the DRE forms an expert opinion on the following:

 

1.Is the person impaired? If so, is the person able to operate a vehicle safely? If the DRE concludes that the person is impaired…

2.Is the impairment due to an injury, illness or other medical complication, or is it drug-related? If the impairment is due to drugs…

3.Which category or combination of categories of drugs is the most likely source of the impairment?

DREs conduct their evaluations in a controlled environment, typically at police precincts, intake centers, troop headquarters or other locations where impaired drivers are transported after arrest. The drug evaluation is not normally done at roadside and is typically a post-arrest procedure.

 

In some cases, the person evaluated will be a driver the DRE personally arrested. In many cases, however, the DRE will be called upon to conduct the evaluation after the driver was arrested by another officer. The DRE is requested to assist in the investigation because of his special expertise and skills in identifying drug impairment.

 

The DRE drug evaluation takes approximately one hour to complete. The DRE evaluates and assesses the person’s appearance and behavior. The DRE also carefully measures and records vital signs and makes precise observations of the person’s automatic responses and reactions. The DRE also administers carefully designed psychophysical tests to evaluate the person’s judgment, information processing ability, coordination and various other characteristics. The DRE will systematically consider everything about the person that could indicate the influence of drugs.

 

The 7 Drug Categories

Physicians have long recognized that different types of drugs affect people differently. Nonetheless, drugs may be categorized or classified according to certain shared symptomatologies or effects. The DRE categorization process is premised on these long-standing, medically accepted facts. DREs classify drugs in one of seven categories: Central Nervous System (CNS) Depressants, CNS Stimulants, Hallucinogens, Phencyclidine (PCP) and its analogs, Narcotic Analgesics, Inhalants, and Cannabis. Drugs from each of these categories can affect a person's central nervous system an impair a person's normal faculties, including a person's ability to safely operate a motor vehicle.

 

(1) Central Nervous System (CNS) Depressants

 

CNS Depressants slow down the operations of the brain and the body. Examples of CNS Depressants include alcohol, barbiturates, anti-anxiety tranquilizers (e.g., Valium, Librium, Xanax, Prozac, and Thorazine), GHB (Gamma Hydroxybutyrate), Rohypnol and many other anti-depressants (e.g., as Zoloft, Paxil).

 

(2) CNS Stimulants

 

CNS Stimulants accelerate the heart rate and elevate the blood pressure and "speed-up" or over-stimulate the body. Examples of CNS Stimulants include Cocaine, "Crack", Amphetamines and Methamphetamine ("Crank").

 

(3) Hallucinogens

 

Hallucinogens cause the user to perceive things differently than they actually are. Examples include LSD, Peyote, Psilocybin and MDMA (Ecstasy).

 

(4) Dissociative Anesthetics

 

One of the seven drug categories. It includes drugs that inhibit pain by cutting off or dissociating the brain's perception of the pain. PCP and it's analogs are examples of Dissociative Anesthetics.

 

(5) Narcotic Analgesics

 

A narcotic analgesic relieves pain, induces euphoria and creates mood changes in the user. Examples of narcotic analgesics include Opium, Codeine, Heroin, Demerol, Darvon, Morphine, Methadone, Vicodin and OxyContin.

 

(6) Inhalants

 

Inhalants include a wide variety of breathable substances that produce mind-altering results and effects. Examples of inhalants include Toluene, plastic cement, paint, gasoline, paint thinners, hair sprays and various anesthetic gases.

 

(7) Cannabis

 

Cannabis is the scientific name for marijuana. The active ingredient in cannabis is delta-9 tetrahydrocannabinol, or THC. This category includes cannabinoids and synthetics like Dronabinol

[man of steel]

So I just went to the pharm.

1. not aware of aride program

2. Sticker releases them from liability

3. It is my resp. to know if I am impared(Self Diagnosis)

4. Advised if I was concerned to get the Med. info. put on back of liscence.There is a box.

5.Could never see a problem if pulled over explain meds. and side effects to officer.

6. I can see a problem if in accident and not even at fault.And I do look different from police.

See law hydrocordone is not tested for.GET SCRIPT>note to self.

I see why kids are having Pharm parties no impared driving!

[AmishRnot4ganja]

Why is it that under every category except cannabis, they list the impairing action of the drug in question, yet under cannabis they list no impairments? What the hell is that about? Have they not yet determined what cannabis's impairing action is, or could it be much more sinister, such as cannabis has no evident impairing action?

 

 

Hello? Hello? (Knocking on head of "law makers") Is there anyone in there with even a modicum of common sense? Have you made a big enough fool of yourself yet, or are you going to continue down the same road and see if you can qualify for "Fool Of The Century"?

 

I personally think they are going for the "Fool Of The Century" title and I hope they win it.

[man of steel]

Marihuana and Driving

 

Marihuana appears in urine and blood 3-5

times more frequently in fatal driving

crashes

???? 60% failed field sobriety test 2 ½ hours

after moderate smoking.

???? 2 joints smoked (10 minutes apart with

1.8-3.6% THC) failed sobriety tests 20minutes later

[Mememe]

The DRE observes the subject’s attitude, coordination, speech, breath and face.

 

Mnemonic device SCAB Face.

[Croppled1]

Marihuana and Driving

 

Marihuana appears in urine and blood 3-5

times more frequently in fatal driving

crashes

???? 60% failed field sobriety test 2 ½ hours

after moderate smoking.

???? 2 joints smoked (10 minutes apart with

1.8-3.6% THC) failed sobriety tests 20minutes later

 

 

Where is this data from I searched and could not find it ? I found this which is from the National Saftey Institute . Similar results are found by studies in other Countries .

 

U.S. DEPARTMENT OF TRANSPORTATION

 

NATIONAL HIGHWAY TRAFFIC SAFETY ADMINISTRATION

 

DOT HS 808 078 NOVEMBER 1993

 

MARIJUANA AND ACTUAL DRIVING PERFORMANCE

 

EFFECTS OF THC ON DRIVING PERFORMANCE

Why do the effects of marijuana appear to be so small?

 

It is a natural question why the effects of marijuana on actual driving performance appear to be so small. As in many previous investigations, subjects attempted to compensate for anticipated adverse effects of marijuana smoking. Our subjects were aware of the impairing effects of THC as shown by lower ratings of perceived driving quality. Consequently, they invested more effort to accomplish the driving tests following THC than placebo. Furthermore, in the car following test, they drove at a greater headway after marijuana smoking; and, in both road tracking and city driving tests, they slightly reduced their driving speed. yet despite their effort, subjects were unable to fully compensate for THC's adverse effects on lateral position variability. This is because SDLP is primarily controlled by an automatic information processing system which operates outside of conscious control. The process is relatively impervious to environmental changes, as shown by the high reliability of SDLP under repeated placebo conditions, but highly vulnerable to internal factors that retard the flow of information through the system. THC and many other drugs are among these factors. When they interfere with the process that restricts SDLP, there is little the afflicted individual can do by way of compensation to restore the situation. Car following and, to a greater extent, city driving performance depend more on controlled information processing and are therefore more accessible for compensatory mechanisms that reduce the decrements or abolish them entirely.

 

That still leaves the question open why performance appears to be more affected by THC in laboratory than actual driving tests. many researchers defend the primacy of laboratory performance tests for measuring drug effects on skills related to driving on the basis of superior experimental control. Certainly some control is always necessary to reduce the confounding influence of extraneous factors that would otherwise so increase measurement error as to totally obscure the drug's effects. however, only some extraneous factors are truly sources of measurement error and others either attenuate or amplify drug effects in real driving and must be considered as relevant to a test's predictive validity. Simply eliminating all of them, first, removes their normal mediating influence on the drug effect, and secondly, affects the subject's motivation to perform the test by making it appear "unreal". Controlling the test usually involves drastic simplification and restriction of response options. The desire in doing this is to isolate a particular driving skill and determine how it changes under the influence of drugs. However, drivers always apply numerous skills in parallel and series. Should one become deficient, they are often able to compensate in a number of ways to achieve a satisfactory level of proficiency. Thus the demonstration of some particular skill decrement in the laboratory in no way indicates that this would ultimately reduce driving safety in reality. Finally there are some skills that simply can not be measured in laboratory tests, at least not easily enough to make it a routine matter. The acquisition of any skill which depends upon automatic information processing requires practice over weeks or months. After learning to drive, subjects possess such skills in abundance and one can only demonstrate how they vary with drug effects in the real task or a very close approximation thereof.

 

Profound drug impairment constituting an obvious traffic safety hazard could as easily be demonstrated in a laboratory performance test as anywhere else. But THC is not a profoundly impairing drug. It does affect automatic information processing, even after low doses, but not to any great extent after high doses. It apparently affects controlled information processing in a variety of laboratory tests, but not to the extent which is beyond the individual's ability to control when he is motivated and permitted to do so in real driving. In short, it would appear as if over-control in laboratory performance tests has resulted in a misimpression of THC's effect, incomplete in some respects and exaggerated in others. The actual driving tests may provide a more realistic impression of the drug's effects, albeit still incomplete and perhaps tending to minimize them with respect to more complex driving situations that come closer to "worst case".

 

The degree of experimental control also varied between driving tests in this series in ways affecting the subjects' motivation. This is illustrated by a comparison between the first and second driving study. The standard road tracking test was applied in both, first in the absence and then in the presence of other traffic. It was only during the former that disturbing observations of two individual's attentional deficits caused the driving instructor to intervene. Driving in the presence of other traffic, subjects were always able to complete the rides without intervention. Lateral position control, an automatic process, did not change as a consequence of the absence or presence of other traffic. What did change was the subjects' motivation to focus attention, a controlled process. Motivation in the second study was very probably affected by recognition of the increased risk of the untoward consequences of wandering attention. This means that the intrinsic motivation produced by the reality of the test situation is an important mediator of THC's effects on performance. Compensatory mechanisms help the driver under the influence of marijuana to maintain an effective level of performance but with an associated cost. If drivers compensate for THC's adverse effects by diminishing driving demands (e.g. by reducing speed and/or increasing headway), this will occur without a reduction in spare capacity. But if they increase effort as well (e.g. by focusing attention), it will occur at the expense of spare capacity. Less capacity would be left for simultaneously performing another task, such as conversing with passengers, using a car telephone, or handling emergency situations. The information processing capacity these situations demand may well go beyond the driver's spare capacity with the result of impaired and perhaps dangerous driving. Results of the present program show that THC increases the mental load of driving, as shown by increased effort ratings and reduced heart rate variability, and consequently reduces spare capacity. This corroborates results from previous simulator and closed-course studies that with reasonable consistency show an adverse THC effect on subsidiary task performance (Smiley, 1986). Further research is required to determine marijuana's effects on actual driving performance when the driver is simultaneously performing another task or suddenly confronted with a situation that requires a rapid adaptive response. The latter was occasionally encountered during the city driving test, but only after a low THC dose. The city driving test should therefore be repeated with subjects consuming higher THC doses.

 

Hazardous driving can also occur in situations that demand very little of the driver's information processing capacity. If the driving task is very monotonous and the demand is low, wandering attention may result in negligent monitoring with disastrous results. This is in fact what happened twice during the driving study on the closed road. After the highest THC dose, one subject failed to shift attention from the prescribed task to an unexpected event (screwdriver on the road); another failed to anticipate a normal event (end of circuit). Though even sober experienced drivers may experience similar deficits, the fact that it happened twice after the highest THC dose, and never after a lower dose or placebo, strongly suggests that drivers under the influence of THC would be unusually susceptible to attentional deficits during prolonged and monotonous driving.

 

How do marijuana's effects on driving performance compare to those of alcohol? There are two sources from which one can draw to answer the question. Information can be directly obtained from studies comparing THC and alcohol effects in the same experiment; and, indirectly, from studies wherein alcohol's effects were assessed using the same methods as applied in the present THC studies. As mentioned in Chapter 1, most closed-course studies on THC also measured alcohol's effects (BACs between 0.04 and 0.10g%). It was generally concluded that THC's effects were less than alcohol's especially at BACs above 0.08g%. The city driving study in the present program also compared the effects of modest doses of alcohol and THC. For doses administered in that study, alcohol produced the greater effects. Indirect evidence concerning the relative effects of THC and alcohol can be obtained from three studies. First, the alcohol calibration study by Louwerens et al. (1985, 1987) which resembled our first driving study in many respects. According to their empirical equation, THC's effects on SDLP were equal to or less than that of BAC = 0.07g%. More recently, studies by Riedel et al. (1989) and Ramaekers et al. (1992a) measured the effects of low doses of alcohol (BACs of 0.05 and 0.03g% respectively) on SDLP. Both groups applied the standard test in the presence of other traffic, as in our second driving study, but on another highway. Mean SDLPs were respectively about 5.0 and 2.5 cm higher while driving after alcohol than placebo. The former elevation is greater than that produced by the highest THC dose in our study. The latter lies between the effects of 200 and 300 ug/kg doses, which were 1.8 and 2.9 cm respectively. There was some discrepancy between alcohol's effects on SDLP in the more recent studies and those predicted by the empirical equation: the former where higher than predicted. The discrepancy appears to be related to the difference between alcohol's effects on the ascending and descending phases of its pharmacokinetic profile. Louwerens measured alcohol's effects at the time when BAC was at the ascending but Riedel and Ramaekers measured them during the descending phase. Notwithstanding methodological differences among studies, both direct and indirect evidence coverage on the conclusion that THC's effects after doses up to 300 ug/kg never exceed alcohol's at BACs of 0.08g%.

 

How do marijuana's effects on driving performance compare to those of drugs other than alcohol? No direct comparisons have ever been made, but many studies employing the standard road tracking test were conducted for measuring other drugs' effects on SDLP during the last decade. The results from a few will be mentioned. Diazepam (Valium) given for one week in a low therapeutic dose (5 mg, thrice daily) caused anxious patients to drive with a mean SDLP about 7 cm higher than their premedication baseline (Van Laar et al., 1992). The same drug and dose given over the same period caused healthy volunteers to drive with a mean SDLP about 6 cm higher than placebo (Van Veggel and O'Hanlon, 1993). Lorazepam (ativan), another anxiolytic, given twice daily for one week in a 1.5 mg dose to healthy volunteers (Volkerts et al., 1988) and a 2 mg dose to patients (Vermeeren et al. 1993), produced an elevation of SDLP of about 10 cm in both cases. Amitriptyline (Elavil), a widely prescribed antidepressant, given in a dose of 50 mg at night and 25 mg in the morning caused healthy volunteers to drive with a mean SDLP about 6 cm higher than placebo (Robbe et al., 1989. Fluraxepam (Dalmane), a hypnotic, was administered to insomniacs and its "hang-over" effects on SDLP were measured 10-11 hours after ingestion. A 15 mg dose of flurazepam elevated mean SDLP by about 4 cm; a 30 mg does, 7 cm. Antihistamines also cause sedation and, consequently, impair road tracking performance. Triprolidine (actifed) increased SDLP by 3.5 cm after a single 5 mg dose (Riedel et al., 1990); and, diphenhydramine 50 mg (Benadryl kapseals) increased SDLP by 4.5 cm (Ramaekers et al., 1992b). This is not to say that all psychotropic drugs produce greater elevations of SDLP than THC. Many in the same and other experiments had less effect than THC did in our studies. These examples are merely cited to indicate that THC's effects as measured in the standard test were in no way unusual. In so far as its effects on SDLP are concerned, THC was just another moderately impairing drug.

 

The foregoing comparisons might be misleading. THC's effects differ qualitatively from many other drugs, especially alcohol. For example, subjects drive faster after drinking alcohol and slower after smoking marijuana (Hansteen et al., 1976/ Casswell, 1979; Peck et al., 1986; Smiley et al., 1987).. Moreover, the simulator study by Ellingstad et al. (1973) showed that subjects under the influence of marijuana were less likely to engage in overtaking maneuvers, whereas those under the influence of alcohol showed the opposite tendency. Very importantly, our city driving study showed that drivers who drank alcohol over-estimated their performance quality whereas those who smoked marijuana under-estimated it. Perhaps as a consequence, the former invested no special effort for accomplishing the task whereas the latter did, and successfully. This evidence strongly suggests that alcohol encourages risky driving whereas THC encourages greater caution, at least in experiments. Another way THC seems to differ qualitatively from many other drugs is that the former users seem better able to compensate for its adverse effects while driving under the influence. Weil et al. (1968) were among the earliest authors who mentioned the possibility that marijuana users can actively suppress the drug's adverse effects. They presumed that THC's effects were confined to higher cortical functions without any general stimulatory or depressive effect on lower brain centers. According to them, the relative absence of neurological, as opposed to psychiatric, symptoms in marijuana intoxication suggests this possibility. More recently, Moskowitz (1985) concluded that the variety of impairments found after marijuana smoking could not be explained by decrements in sensory or motor functions which led him to hypothesize that some important central cognitive process is impaired by THC, without saying what it is. Identification of THC's site of action would greatly enhance our understanding of the drug's psychopharmacological effects.

 

Epidemiological research has shown that THC is infrequently detected in the blood of fatally injured drivers as the only drug present. In most cases alcohol is also detected. The effects of the combination of THC and alcohol on actual driving performance have never been studied in the presence of other traffic. Closed-course studies have shown that the effects of both drugs, when taken in combination, are generally additive (Atwood et al., 1981; Peck et al., 1986). This may only be so for those behaviors that are similarly affected by both rugs given separately. Closer examination of the combined use is warranted in those driving situations where both drugs produce qualitatively different effects. It may well be so that alcohol reduces drivers' insight or motivation to the point where they would no longer attempt to compensate for the THC effect. As a result, the combined effects on drivers' performance could well be greater than the sum of either drug acting separately. There is therefore a great need for further research on marijuana and actual driving research, but now extended to the combination of marijuana and alcohol.

 

In summary, this program of research has shown that marijuana, when taken alone, produces a moderate degree of driving impairment which is related to the consumed THC dose. The impairment manifests itself mainly in the ability to maintain a steady lateral position on the road, but its magnitude is not exceptional in comparison with changes produced by many medicinal drugs and alcohol. Drivers under the influence of marijuana retain insight in their performance and will compensate where they can, for example, by slowing down or increasing effort. As a consequence, THC's adverse effects on driving performance appear relatively small. Still we can easily imagine situations where the influence of marijuana smoking might have an exceedingly dangerous effect; i.e., emergency situations which put high demands on the driver's information processing capacity, prolonged monotonous driving, and after THC has been taken with other drugs, especially alcohol. We therefore agree with Moskowitz' conclusion that "any situation in which safety both for self and others depends upon alertness and capability of control of man-machine interaction precludes the use of marijuana". However, the magnitude of marijuana's, relative to many other drugs', effects also justify Gieringer's (1988) conclusion that "marijuana impairment presents a real, but secondary, safety risk; and that alcohol is the leading drug-related accident risk factor". Of the many psychotropic drugs, licit and illicit, that are available and used by people who subsequently drive, marijuana may well be among the least harmful. Campaigns to discourage the use of marijuana by drivers are certainly warranted. But concentrating a campaign on marijuana alone may not be in proportion to the safety problem it causes.

 

 

 

 

DRUG PLASMA CONCENTRATIONS AND DRIVING PERFORMANCE

One of the program's objectives was to determine whether it is possible to predict driving impairment by plasma concentrations of THC and/or its metabolite, THC-COOH, in single samples. The answer is very clear: it is not. Plasma of drivers showing substantial impairment in these studies contained both high and low THC concentrations; and, drivers with high plasma concentrations showed substantial, but also no impairment, or even some improvement. The first driving study showed that impairment in the road tracking test was nearly the same in the first and second test, executed between 40-60 and 100-120 minutes after initiation of smoking, respectively. Plasma concentrations of THC and THC-COOH, however, were not the same during the tests: both were lower during the second than the first. The same pattern was found for ratings of perceived "high". It has been said that behavioral signs of intoxication, though small, outlast physiological and subjective reactions to THC (Reeve et al. 1983; Yesavage et al., 1985). to examine this hypothesis, future research should extend actual driving performance measurements to 4, 8, 16 and 24 hours after smoking. If driving impairment still occurs after THC disappears from plasma, it could mean that previous epidemiological research has underestimated the proportion of drivers who were driving under the influence of marijuana at the times their accidents occurred.

 

Mean speed was the only measure of driving performance that was even moderately related to plasma concentrations of the drug. Subjects with higher THC concentrations in plasma drove slower in the standard road tracking test (correlations varying from r = -.18 to r = -.72 between conditions). This effect might have been even more pronounced if the subjects had not been instructed to drive at a particular speed, and if they had had no feedback from the speedometer.

 

 

 

CONCLUSIONS

The major conclusions from the present program are summarized as follows:

* Current users of marijuana prefer THC doses of about 300 ug/kg to achieve their desired "high".

* It is possible to safely study the effects of marijuana on driving on highways or city streets in the presence of other traffic.

* Marijuana smoking impairs fundamental road tracking ability with the degree if impairment increasing as a function of the consumed THC dose.

* Marijuana smoking which delivers THC up to a 300 ug/kg dose slightly impairs the ability to maintain a constant headway while following another car.

* A low THC dose (100 ug/kg) does not impair driving ability in urban traffic to the same extent as a blood alcohol concentration (BAC) of 0.04g%.

* Drivers under the influence of marijuana tend to over-estimate the adverse effects of the drug on their driving quality and compensate when they can; e.g. by increasing effort to accomplish the task, increasing headway or slowing down, or a combination of these.

* Drivers under the influence of alcohol tend to under-estimate the adverse effects of the drug on their driving quality and do not invest compensatory effort.

* The maximum road tracking impairment after the highest THC dose (300 ug/kg) was within a range of effects produced by many commonly used medicinal drugs and less than that associated with a blood alcohol concentration (BAC) of 0.08g% in previous studies employing the same test.

* It is not possible to conclude anything about a driver's impairment on the basis of his/her plasma concentrations of THC and THC-COOH determined in a single sample.

 

[+EdwardGlen]

Marihuana and Driving

 

Marihuana appears in urine and blood 3-5

times more frequently in fatal driving

crashes

60% failed field sobriety test 2 ½ hours

after moderate smoking.

2 joints smoked (10 minutes apart with

1.8-3.6% THC) failed sobriety tests 20minutes later

 

But not the primary cause of the fatal accidents! This statement has been around for a few years now and is very misleading to say the least.

 

Didn't schuette use this or a similar 'fact' a week or so ago...

[+EdwardGlen]

Marihuana and Driving

 

Marihuana appears in urine and blood 3-5

times more frequently in fatal driving

crashes

???? 60% failed field sobriety test 2 ½ hours

after moderate smoking.

???? 2 joints smoked (10 minutes apart with

1.8-3.6% THC) failed sobriety tests 20minutes later

 

But not the primary cause of the fatal accidents. This statement has been around for a few years now and is very misleading to say the least.

 

Didn't schuette use this or a similar 'fact' a week or so ago...

[man of steel]

An Update on

Michigan’s

Medical

Marihuana Act

Presented by:

Kenneth Stecker

Prosecuting Attorneys Association of Michigan

I really believe that this will be the powerpoint used to guide the senate

and house. Please read it. It is the most spelled out plan of the AG and prosecuters.

I would question how they came up with the results.

I don't smoke two joints in 10 min.

Did they hook a monkey to a gas mask?

Maybee Bill did the test?

[tooldini]

2 joints in 10 minutes I would not be walking LOL I would be sleeping for days