Sweat bleaching clothes.

[Guest guest]

Hi All,

 

Normal sweat is acidic (pH varying from <5 to circa 6.5, with an extreme

range of circa 4.2 to 7.5).

 

Sweat pH varies widely with physiological activity (exercise, sweating rate),

gender and disease.

 

Female sweat tends to have higher pH than male sweat.

 

Males with diseases causing feminisation may have sweat with higher pH

than " normal " males?

 

Panic attacks & hyperventilation can induce alkalosis and change sweat pH.

 

Sweat pH is lower at low sweating rates than at high sweating rates.

 

However, sweat contains urea and some skin bacteria can convert urea to

ammonia.

 

Biosensors are being developed for embedding in " smart clothes " to

continualy monitor sweat composition, including sweat pH. See:

http://tinyurl.com/5nacr6

 

Some abstracts are below.

 

Best regards,

 

 

http://tinyurl.com/59wpmm says that the normal pH of sweat is less than 5

(viz acidic). [Determination of Vitality From A Non-Invasive Biomedical

Measurement for Use in Integrated Biometric Devices Reza Derakhshani,

B.S.E.E. THESIS Submitted to Dept of Computer Science and Electrical

Engineering of the College of Engineering and Mineral Resources at WEST

VIRGINIA UNIVERSITY]

 

Nikolajek WP, Emrich HM. pH of sweat of patients with cystic fibrosis. Klin

Wochenschr. 1976 Mar 15;54(6):287-8. pH of the sweat from patients with

cystic fibrosis and in controls was measured as a function of the sweat-rate

using a fluorescence-pH-indicator (umbelliferone). In both populations sweat

is acid at low sweat-rates and alkaline at high ones. The results do not

favour an abnormality of the ductal H+-secretion as the pathomechanism of

cystic fibrosis. PMID: 4645 [PubMed - indexed for MEDLINE]

 

Burry JS, Coulson HF, Esser I, Marti V, Melling SJ, Rawlings AV, Roberts G,

Mills AK. Erroneous gender differences in axillary skin surface/sweat pH. Int

J Cosmet Sci. 2001 Apr;23(2):99-107. Unilever Research, Port Sunlight

Laboratory, Quarry Rd East, Bebington, Wirral, U.K. Assessing accurately

the pH of axillary eccrine sweat is of vital importance in the antiperspirant

industry. Eccrine sweat pH is a critical parameter in determining the

effectiveness of antiperspirants; antiperspirant salts dissolve in sweat and

diffuse into the sweat glands, where the resultant acidic solution hydrolyses

in more alkaline sweat forming an amorphous metal hydroxide gel, thereby

restricting the flow of eccrine sweat. Comparison of the skin surface and

sweat pH of males and females reported in the literature shows that,

although consistent male/female differences have been observed on the

forearm, determination of significant gender-based pH differences across

other sites are less conclusive. Studies on the back and infra-mammary

regions exhibited significant gender differences in skin surface pH, whereas

those on the forehead, cheek, neck and inguinal area showed no such

difference. With regard to the axilla specifically, four studies have been

reported, three showing no significant difference in axillary skin surface pH

and one indicating that females have an eccrine sweat pH of 7 and males

have a sweat pH of 5.6. This paper describes a series of carefully controlled

studies aimed at assessing potential gender differences in eccrine sweat

and skin surface pH following exposure to a variety of temperature, humidity

and time conditions. The results highlight the importance of controlling

precisely the time of investigation, site of measurement and, most

importantly, the necessity to pre-equilibrate samples in 40 mmHg carbon

dioxide (equivalent to arterial CO(2) tension (pCO2)) before determining

sweat pH. When these parameters are controlled no gender differences in

axillary sweat or skin surface pH are observed. Large differences in eccrine

sweat and skin surface pH are found, however, between the vault (hairy

region) and fossa (non-hairy region) of the axilla. PMID: 18498454 [PubMed

- in process]

 

Meyer F, Laitano O, Bar-Or O, McDougall D, Heigenhauser GJ. Effect of

age and gender on sweat lactate and ammonia concentrations during

exercise in the heat. Braz J Med Biol Res. 2007 Jan;40(1):135-43. Erratum

in: Braz J Med Biol Res. 2007 Jun;40(6):885. Heingenhauser, G J F

[corrected to Heigenhauser, G J F]. Laboratório de Pesquisa do Exercício,

Escola de Educação Física, Universidade Federal do Rio Grande do Sul,

Porto Alegre, RS, Brasil. The dependence of sweat composition and acidity

on sweating rate (SR) suggests that the lower SR in children compared to

adults may be accompanied by a higher level of sweat lactate (Lac-) and

ammonia (NH3) and a lower sweat pH. Four groups (15 girls, 18 boys, 8

women, 8 men) cycled in the heat (42 degrees C, 20% relative humidity) at

50% VO2max for two 20-min bouts with a 10-min rest before bout 1 and

between bouts. Sweat was collected into plastic bags attached to the

subject's lower back. During bout 1, sweat from girls and boys had higher

Lac- concentrations (23.6 +/- 1.2 and 21.2 +/- 1.7 mM; P < 0.05) than sweat

from women and men (18.2 +/- 1.9 and 14.8 +/- 1.6 mM, respectively), but

Lac- was weakly associated with SR (P > 0.05; r = -0.27). Sweat Lac-

concentration dropped during exercise bout 2, reaching similar levels among

all groups (overall mean = 13.7 +/- 0.4 mM). Children had a higher sweat

NH3 than adults during bout 1 (girls = 4.2 +/- 0.4, boys = 4.6 +/- 0.6, women

= 2.7 +/- 0.2, and men = 3.0 +/- 0.2 mM; P < 0.05). This difference persisted

through bout 2 only in females. On average, children's sweat pH was lower

than that of adults (mean +/- SEM, girls = 5.4 +/- 0.2, boys = 5.0 +/- 0.1,

women = 6.2 +/- 0.5, and men = 6.2 +/- 0.4 for bout 1, and girls = 5.4 +/- 0.2,

boys = 6.5 +/- 0.5, women = 5.2 +/- 0.2, and men = 6.9 +/- 0.4 for bout 2).

This may have favored NH3 transport from plasma to sweat as accounted

for by a significant correlation between sweat NH3 and H+ (r = 0.56). Blood

pH increased from rest (mean +/- SEM; 7.3 +/- 0.02) to the end of exercise

(7.4 +/- 0.01) without differences among groups. These results, however,

are representative of sweat induced by moderate exercise in the absence of

acidosis. PMID: 17225006 [PubMed - indexed for MEDLINE]

 

Patterson MJ, Galloway SD, Nimmo MA. Effect of induced metabolic

alkalosis on sweat composition in men. Acta Physiol Scand. 2002

Jan;174(1):41-6. Strathclyde Institute for Biomedical Sciences, University of

Strathclyde, Glasgow, Scotland, UK. To determine whether induced

metabolic alkalosis affects sweat composition, 10 males cycled for 90 min at

62.5 +/- 1.3% peak oxygen uptake, on two separate occasions. Subjects

ingested either empty capsules (placebo) or capsules containing NaHCO3-

(0.3 g kg-1 body mass; six equal doses) over a 2-h period, which

commenced 3 h prior to exercise. Arterialized-venous blood samples were

drawn prior to and after 15, 30, 60 and 90 min of exercise. Sweat was

aspirated at the end of exercise from a patch located on the right scapula

region. NaHCO3- ingestion elevated blood pH, [HCO3-] and serum [Na+],

whereas serum [Cl-] and [K+] were reduced, both at rest and during exercise

(P < 0.05). Sweat pH was greater in the NaHCO3- trial (6.24 +/- 0.18 vs.

6.38 +/- 0.18; P < 0.05), whereas sweat [Na+] (49.5 +/- 4.8 vs. 50.2 +/- 4.3

mEq L-1), [Cl-] (37.5 +/- 5.1 vs. 39.3 +/- 4.2 mEq L-1) and [K+] (4.66 +/- 0.19

vs. 4.64 +/- 0.34 mEq L-1) did not differ between trials (P > 0.05). Sweat

[HCO3-] (2.49 +/- 0.58 vs. 3.73 +/- 1.10 mEq L-1) and [lactate] (8.92 +/- 0.79

vs. 10.51 +/- 0.32 mmol L-1) tended to be greater after NaHCO3- ingestion,

although significance was not reached (P=0.07 and P=0.08, respectively).

These data indicate that induced metabolic alkalosis can modify sweat

composition, although it is unclear whether the secretory coil, reabsorptive

duct, or both are responsible for this alteration. PMID: 11851595 [PubMed -

indexed for MEDLINE]

 

Platzek T, Lang C, Grohmann G, Gi US, Baltes W. Formation of a

carcinogenic aromatic amine from an azo dye by human skin bacteria in

vitro. Hum Exp Toxicol. 1999 Sep;18(9):552-9. Federal Institute for Health

Protection of Consumers and Veterinary Medicine, Postfach 330013, D-

14191 Berlin, Germany. Azo dyes represent the major class of dyestuffs.

They are metabolised to the corresponding amines by liver enzymes and the

intestinal microflora following incorporation by both experimental animals

and humans. For safety evaluation of the dermal exposure of consumers to

azo dyes from wearing coloured textiles, a possible cleavage of azo dyes by

the skin microflora should be considered since, in contrast to many dyes,

aromatic amines are easily absorbed by the skin. A method for measuring

the ability of human skin flora to reduce azo dyes was established. In a

standard experiment, 3x10(11) cells of a culture of Staphylococcus aureus

were incubated in synthetic sweat (pH 6.8, final volume 20 mL) at 28

degrees C for 24 h with Direct Blue 14 (C.I. 23850, DB 14). The reaction

products were extracted and analysed using HPLC. The reduction product

o-tolidine (3,3'-dimethylbenzidine, OT) could indeed be detected showing

that the strain used was able to metabolise DB 14 to the corresponding

aromatic amine. In addition to OT, two further metabolites of DB 14 were

detected. Using mass spectrometry they were identified as 3,3'-dimethyl-4-

amino-4'-hydroxybiphenyl and 3, 3'-dimethyl-4-aminobiphenyl. The ability to

cleave azo dyes seems to be widely distributed among human skin bacteria,

as, under these in vitro conditions, bacteria isolated from healthy human skin

and human skin bacteria from strain collections also exhibited azo reductase

activity. Further studies are in progress in order to include additional azo

dyes and coloured textiles. At the moment, the meaning of the results with

regard to consumer health cannot be finally assessed. PMID: 10523869

[PubMed - indexed for MEDLINE]

 

Alvear-Ordenes I, García-López D, De Paz JA, González-Gallego J. Sweat

lactate, ammonia, and urea in rugby players. Int J Sports Med. 2005

Oct;26(8):632-7. Department of Physiology, University of León, Campus

Universitario, León, Spain. The purpose of this study was to investigate

sweat lactate, ammonia, and urea excretion in rugby players. Fifteen elite

amateur rugby players volunteered to participate. The study was conducted

during competitive matches in the official season. Plasma and sweat

concentrations of lactate, ammonia, and urea were measured before and

after the matches. Peak values for creatine kinase activity were observed 24

h after the match. There was no significant change between time points for

blood lactate concentration but secretion rate per unit surface and time was

significantly reduced after the match. Sweat ammonia concentration

increased significantly during the match; values were significantly reduced

after 24 h and still remained low at 72 h. Secretion rate was also reduced

from 24 h. Urea concentration was significantly reduced at 48 h, while

secretion rates decreased at 24 h and 48 h. Lactate in blood was

significantly elevated during the match but not thereafter. Blood ammonia

was significantly elevated during the match and did not differ from the

resting values at 24 or 48 h. Urea in blood tended to decrease during the

match, with a significant reduction at 24 h. Significant positive correlations

were observed between blood and sweat concentrations for urea and

ammonia but not for lactate. Sweat rate correlated positively with sweat

lactate secretion. The fact that part of the ammonia formed during exercise

is lost with sweat indicates the importance of the purine nucleotide cycle

during rugby matches. Our data also confirm that sweat lactate

concentration is not influenced by circulatory blood lactate

in rugby players. PMID: 16158367 [PubMed - indexed for MEDLINE]

 

Janszky I, Szedmák S, Istók R, Kopp M. Possible role of sweating in the

pathophysiology of panic attacks. Int J Psychophysiol. 1997 Dec;27(3):249-

52. Institute of Behavioural Sciences, Semmelweis University of Medicine,

Budapest, Hungary. In recent years the role of hyperventilation in the

generation of panic attacks has attracted a considerable amount of interest.

According to these studies hyperventilation can elicit the somatic symptoms

of panic due to systemic alkalosis. We suggest that since in the case of

panic, sweating might cause alkalosis, it could also contribute to the

generation of panic attacks. In light of this hypothesis we made a statistical

analysis of the panic symptoms of 111 panic patients diagnosed according

to DSM-III criteria. The analysis revealed that: (1) there was a well identified

group of panic patients who had minor breathing difficulties with heavy

sweating; and (2) that all the patients sampled had either severe breathing,

or sweating symptoms, or both. We conclude that in the absence of the

intensive physical activity of the 'flight or fight' reaction, sweating as well

as

hyperventilation can cause alkalosis, which in turn might generate panic

attacks. PMID: 9451583 [PubMed - indexed for MEDLINE]