Mild headache

NuvaRing use as directed (discontinued 8 months ago) Acetaminophen 325 mg 2 tablets every 4 to 6 hours as needed for mild headaches... 

Here you can still use the Pearson chi-square test as shown in the 2x2 table example as long as your response variable is nominal and merely descriptive. If your response variable is ordinal, meaning that it is an ordered sequence, and you can use a parametric test, then you should use the Mantel-Haenszel test statistic for parametric tests of association. For instance, if in our previous example the variable called headache was coded as a 2 when the patient experienced extreme headache, a 1 if mild headache, and a 0 if no headache, then headache would be an ordinal variable. You can get the Mantel-Haenszel /pvalue by running the following SAS code ... 

Options for adjuvant hormonal therapy in postmenopausal women include aromatase inhibitors (e.g. anastrozole, letrozole, or exemestane) either in place of or after tamoxifen. Adverse effects with aromatase inhibitors include hot flashes, myalgia/arthralgia, vaginal dryness/atrophy, mild headaches, and diarrhea. 

The AEGL-1 values were based on concentrations at 0.5 ppm and 0.1 ppm, which were the thresholds for mild headaches in healthy individuals at exposure durations of 1 and 6 h, respectively (Stewart et al. 1974). This effect can be considered the threshold for mild discomfort (only one subject was affected at each exposure), which falls within the definition of an AEGL-1. The 0.5-ppm concentration was used to derive the 30-min and 1-h AEGL-1 values, and the 0.1-ppm concentration was used for the 4- and 8-h values. Because the time and concentration values were based on the most susceptible subject, these concentrations were adjusted by an uncertainty factor (UF) of 3 to account for potential differences in human sensitivity and scaled to the appropriate time periods using the C xt=k relationship. A UF of 3 was considered sufficient as no susceptible populations were identified (the headache effect is the same as that experienced by patients medicated with nitro... 

Testing of the subjects consisted of both subjective evaluations and physiological and central nervous system responses observed under medical supervision. The lowest concentration at which odor was detected was 0.2 ppm (four of nine subjects), but the ability to detect the odor disappeared within 5 min. Subjective symptoms consisted of headache and eye irritation. At 0.1 ppm, two of the subjects experienced mild headache (Table 2-3). One of these subjects had developed headache during each of the control exposures and during the exposure at 0.03 ppm. The other subject developed headache after 6 h, and the headache continued for several hours postexposure. 

Of the nine subjects exposed at 0.21-0.26 ppm (18 exposures all nine subjects took part in the 8-h exposures, and three of the nine were exposed for 8 h on two separate occasions), seven developed headaches of varying intensity. The headaches were mild in intensity for two of three subjects during the 2-h exposure. During the twelve 8-h exposures, there were five incidences of mild headache and six incidences of severe headache. The number of subjects in each category of headache could not be ascertained from the data. The... 

At 0.35 ppm, all three subjects exposed for 2 h developed mild headaches, and one of three subjects exposed for 8 h developed a mild headache. Two of three subjects exposed for 8 h developed severe headaches. One subject also developed slight eye irritation, which persisted throughout the 2 h exposure. Four of the nine subjects detected the odor of the compound, which they described as mild at this concentration however, the odor was not detectable after 5 min of exposure. The morphology of the visual evoked response, while variable, was altered, particularly in three subjects exposed for 8 h. The exposure produced an increase in the peak-to-peak amplitude of the 3-4—5 wave complex. The authors interpreted the VER changes as consistent with the VER changes produced by central nervous system depression. 

PGDN has effects on the cardiovascular and central nervous systems. Exposure of healthy, primarily male subjects to PGDN at a concentration of 0.03 ppm for 8 h was without adverse effects. A mild headache was present in one of three subjects after exposure at 0.1 ppm for 6 h. Adverse effects became more severe at higher concentrations and shorter exposure durations 0.2 ppm for 8 h produced severe headache in six of 12 exposures 0.35 ppm for 8 h produced severe headache in two of three subjects and disturbance of... 

Data from the study by Stewart et al. (1974) suggest that the relationship between exposure concentration and exposure duration for end points of both mild and severe headaches is approximately linear (i.e., mild headaches induced by 6, 2, 2, and 1 h at exposure concentrations of 0.1, 0.2, 0.3, and 0.5... 

Occupational exposures and the study with human volunteers indicate that exposures at low concentrations cause headaches and signs of central nervous system depression. No headaches were reported and no equilibrium disturbances were measured during occupational exposures of healthy workers to Otto Fuel II (measured as PGDN) at concentrations <0.22 ppm (average of approximately 0.06 ppm) for periods of 30-60 min, although subtle changes in eye movements were recorded (Horvath et al. 1981). In a study with healthy but previously unexposed male volunteers, the threshold for odor detection was 0.2 ppm (Stewart et al. 1974). Mild headaches were reported in one of three subjects after a 6-h exposure at 0.1 ppm, in two of three subjects after a 2-h exposure at 0.2 ppm, and in one of three subjects after a 1-h exposure at 0.5 ppm. Severe headaches occurred after an 8-h exposure at 0.2... 

The study by Stewart et al. (1974) with human volunteers is relevant to the derivation of AEGL-1 values. Within the definition of an AEGL-1, both healthy and susceptible individuals could experience mild discomfort. A mild headache can be considered mild discomfort and the threshold concentration-time at which one or more subjects first developed a mild headache was used to derive the AEGL-1 values. No subjects (other than the one that developed a headache during the control sessions) developed headaches during an 8-h exposure at 0.03 ppm. The highest concentrations and exposure durations that did not result in headache and the lowest concentrations and exposure durations that resulted in mild headaches are as follows ... 

End point/Concentration/Rationale Threshold for mild headache in 1 of 3 subjects after a 6-h exposure at 0.1 ppm and after a 1-h exposure at 0.5 ppm. The threshold for mild headache falls within the AEGL-1 definition of mild discomfort. 

Time scaling Cnxt=k where n=l (k=0.167 ppm-hour for the 30-min value and 0.2 ppm-h for the 4- and 8-h values). Data from the key study suggest that the relationship between exposure concentration and exposure duration for end points of both mild and severe headaches is approximately linear (i.e., mild headaches induced by 6, 2, 2, and 1 h at exposure concentrations of 0.1, 0.2, 0.3, and 0.5 ppm, respectively, and severe headaches induced at 8, 8, 2, and 1 h at exposure concentrations of 0.2, 0.3, 0.5, and 1.5 ppm, respectively). The concentrationxtime product is approximately 0.5 for mild headaches and approximately 1.6 for severe headaches. The linear relationship is consistent with an n value of 1 in the relationship between concentration and time, Cnxt=k. The 1 -h value was used to extrapolate to the shorter duration (30 min) and the 6-h value was used to extrapolate to the longer durations (4 and 8 h). The 10-min value was set equal to the 30-min value. 

Toxicity end point Maehlyand Swensson 1970 No adverse effect in healthy adult humans occupationally exposed at geometric mean concentration of <1 (range 0.01-3.3 ppm, personal samplers [up to 6 ppm, area samples]) or 5 ppm mild headache in adult humans occupationally exposed at 8 ppm. The exposure duration was considered to be 8 h. 

Effects No exposure related adverse symptoms or health effects (surveys and medical examinations taken in spring and fall of year) (Leeser et al. 1990) mild headache, other symptoms (El Ghawabi et al. 1975) no effects reported (Grabois 1954 Maehly and Swensson 1970 Hardy et al. 1950). 

Data adequacy The preponderance of data from the key studies support an 8-h noeffect concentration of 1 ppm. The Leeser et al. (1990) study encompassed subjective symptoms as well as extensive medical examinations. The occupational monitoring study of El Ghawabi et al. (1975), in which it is believed that workers inhaling a mean concentration of 8 ppm may suffer mild headaches, supports the safety of the derived values. The values are also supported by a NIOSH (1976) report in which 5 ppm was identified as a no-effect concentration in the Grabois et al. (1954) occupational study. Additional monitoring studies support the values. ... 

Initial exposure to NG (or NG EGDN mixmres where exposures are considered additive) characteristically results in an intense, throbbing headache that begins in the forehead and moves to the occipital region. Volunteers developed mild headaches when exposed to NG EGDN vapor at concentrations of 0.5mg/m for 25 minutes. It has been suggested that at least some workers may develop headaches at concentrations as low as 0.1 mg/mk ... 

Neuroendocrine measures (Newhouse et al. 1990] tended to confirm that the doses used were active at CNS nicotinic receptors. Adrenocorticotropic hormone and cortisol showed significant (F <. 01] dose- and time-related increases in both groups of subjects. The adrenocorticotropic hormone increase was evident by 30 minutes, with the cortisol increase being delayed until 60 minutes, suggesting no direct effect of nicotine on adrenal cortical cells. Reports of physical side effects were generally minimal, although some subjects complained of a mild headache. No consistent report of nausea was found in either group. 

Adverse effects include injection site soreness, redness and swelling mild headache, malaise, fatigue, fever, nausea and loss of appetite. 

Explosives have an abundance of toxicological hazards, the extent of which is being increasingly identified. Due to their chemical structure, most explosives are toxic to some extent. Since the effect of toxicity may vary from a mild headache to serious damage of internal organs, toxicity in military explosives should be contained to a minimum level. Any explosive of high toxicity is unacceptable for military use. 

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